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This was going to be a simple confession about my addiction to pens and the joy that I have had in liberating them from stationery cupboards and conference stands around the world but when I cam to take a photograph of those on my desk in my study the realization suddenly hit me that I have several other things that I could confess to and the evidence for these is for all to see in my study.
This is part of my desk, about half of it is shown here. I bought it in Habitat some 25 years ago when the Black Ash finish was trendy and I still like it. The simple answer to "why are there 2 PC on your desk?" is "Because the third is downstairs in the living room". By coincidence they are all IBM Thinkpads. Also in the picture are three mobile phones, again for good reasons.
The discerning viewer may be able to tell that between the two PCs are 5 pen pots, all from Muji, and a desk tidy with three pen compartments. A quick count makes that over 120 pens, and that does not include those in the two pencil cases just about visible on the left edge of the picture, nor does it count those in the rest of the house where Muji pen holders are more common that light bulbs.
This view of my study is far too revealing!
The piles of comics on the floor should not be a surprise to anyone, nor should the two long boxes of comics behind them. The other boxes of comics are elsewhere in the room. In the bookcase at the back of the picture are graphic novels, e.g. Sandman, Daredevil and Dreadstar. My plan is to get some custom built shelving, probably System 180 stuff (I have a lot of this including a desk, a wardrobe and a bed), to keep all my comics in but I need to do some work to design them first.
Also in the bookcase are a few books. Most of them are old, battered and written by Leslie Charteris and featuring The Saint. Hopefully the rumors of a new TV series will come true this year.
What looks as though it might be a black bag in the middle of the picture is, in fact, fourteen black bags in the middle of the picture, and there are at least seven other bags spread around the room. My addiction to cheap bags with corporate logos on is probably even worse than that for cheap pens with corporate logos on.
I could not show you the big bookcase in the room, nor the filing cabinet in the desk, otherwise I would have to explain why I need so much A4 paper that either has a corporate logo on each page or which has been nicely bound into a book with a corporate logo on the cover.
Time to go to the pub and think about things!
9 January 2008
You can tell a lot about a man from his study
More stories like this: the_saint
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Pakodas are loved by all throughout the year, but they gain a special significance in the monsoon, which is in fact the perfect weather to enjoy crispy, steaming hot stuff right out of the kadhai! Just the warmth of the hot oil in the kadhai together with the aroma of spices can be soul-warming on a wet and cold day. A cozy weekend at home can become all the more special when evening tea is accompanied by pakodas made with love. Pakodas can add to the joy of chatting with teammates or huddling together with friends and watching a movie. Shed your inhibitions, wrap some hot pakodas in a paper cover, go out and share them with the kids in your neighbourhood, while you make paper boats for them! Indeed, pakodas are not just spicy, crunchy snacks; they are part-and-parcel of our monsoon culture and a trigger for childhood memories, of happy, carefree times!
We have put together a couple of our favourite pakodas and bhajiyas for you to enjoy. From the ever popular Moong Dal Pakoda, Peanut Pakoda and Banana Bhajiya to tongue-tickling ones like the Methi Pakoda and seasonal ones like the Yam Fritters and Kand Aloo Pakoda, we have given you a wide choice to pick from. Innovative recipes like the Khichdi Pakodas and the Rice and Peanut Pakoda also give you a chance to use up leftovers while surprising your family with delectable crispies.
Make sure you serve the pakodas piping hot with a cup of hot beverage and lots of love.
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subset: commoncrawl


text:
For your convenience, we have included the definitions to some of the most common, and often confusing, mortgage terms.
100% loan
A loan with no down payment. The loan amount equals the property value.
Adjustable-rate mortgage (ARM)
A mortgage with an interest rate that adjusts periodically based on a preselected index, causing interest rates and payments to rise and fall with the market.
Adjustment interval
The time between changes in the interest rate and monthly payments on an ARM.
Agreement of sale
Also known as a "sales contract," a written document in which a purchaser agrees to buy property under certain given conditions, and the seller agrees to sell under certain given conditions.
A monthly repayment schedule in which a loan is repaid in fixed payments of principal and interest.
Annual percentage rate (APR)
The annual cost of a loan, expressed as a yearly rate. APR takes into account interest, discount points, lender fees and mortgage insurance, so it will be slightly higher than the interest rate on the loan.
Often referred to as a 1003, an initial statement of personal and financial information required to approve your loan.
A written estimate of a property's current market value, based on recent sales information for similar properties, the current condition of the property and how the neighborhood might affect future property value.
ARM disclosure
An additional disclosure specific to adjustable-rate mortgages that must be prepared and presented to the consumer at application whenever an adjustable-rate mortgage transaction is contemplated (Note: home equity lines have their own unique disclosure).
ARM handbook
The Consumer Handbook to Adjustable-Rate Mortgages ("CHARM" booklet) must be presented to the consumer when applying for an ARM loan (in addition to the ARM disclosure referenced above).
A local tax levied against properties that have benefited from civil improvements such as road or sidewalk construction, a sewer or street lights.
Anything of monetary value that a person owns. Assets include real property, personal property and enforceable claims against others (including bank accounts, stocks, mutual funds and so on).
Proclamation by a court of an individual's (or organization's) state of insolvency, or inability, to pay debts. Petition may be brought by an individual or his creditors, with a goal of orderly and equitable settlement of obligations.
Basis point
A unit of measure: 1/100th of one percent. For example, the difference between a 9.0 percent loan and a 9.5 percent loan is 50 basis points.
Biweekly mortgage
A payment plan under which one pays one-half of a monthly payment every two weeks, saving interest substantially over the life of the loan.
Borrower (Mortgagor)
An individual who applies for and receives a loan in the form of a mortgage with the intention of repaying the loan in full.
An individual who assists in arranging funding or negotiating contracts for a client, but does not loan money himself.
A situation in which the seller contributes money that allows the lender to give the buyer a lower rate and payment, usually in exchange for an increase in sales price. With a refinance, this could be paid by the borrower.
Limits on changes in ARM interest rates or monthly payments, either in an adjustment period or over the life of the loan.
A refinance for more than the balance of the original mortgage, with the extra money is taken out of the equity in the property.
Certificate of title
Written opinion of the status of title to a property, given by an attorney or title company. This certificate does not offer the protection given by title insurance.
Closing (or settlement)
Meeting between the buyer, seller and lender or their agents at which property and funds legally change hands.
Closing costs
Fees incurred in a real estate or mortgage transaction and paid by borrower and/or seller during a mortgage loan closing. These typically include a loan origination fee, discount points, attorney's fees, title insurance, appraisal, survey and any items that must be prepaid, such as taxes and insurance escrow payments. The cost of closing is usually about 3 to 6 percent of the mortgage amount.
Closing disclosure
This disclosure replaced the HUD1 Settlement Statement and the final Truth-in-Lending disclosure. The disclosure reflects the actual terms and costs associated with the loan transaction and must be provided to the borrower three business days before consummation of the loan.
Closing statement
A financial disclosure statement that lists the funds received and expected at the closing.
Assets that back a mortgage loan.
A formal offer by a lender to make a loan under certain terms or conditions to a borrower.
Consumer Financial Protection Bureau (CFPB)
A federal agency that enforces laws that protect consumers of financial products and services such as mortgages, credit cards and deposit accounts.
A condition that must be satisfied before a contract is legally binding before a sale can close.
Contract of sale
The agreement between the buyer and seller on the purchase price, terms and conditions of a sale.
Conventional loan
A mortgage not insured by the FHA or guaranteed by the VA.
Credit report
A report detailing the credit history of a prospective borrower, used when determining creditworthiness.
Debt-to-income ratio
The ratio, expressed as a percentage, that results when a borrower's monthly payment obligation on long-term debts is divided by monthly income.
A legal document that transfers a property from one owner to another. The deed contains a description of the property, and is signed, witnessed and delivered to the buyer at closing.
Deed of trust
Agreement to pledge property as security for a loan, used in many states in place of a mortgage. In this arrangement, the borrower transfers legal title to a trustee who holds the property in trust as security for the repayment of the debt. The deed of trust becomes void if the debt is repaid, but if the borrower defaults on the loan, the trustee may sell the property to pay the debt.
Cash paid when a formal sales contract is signed. The deposit is usually held by a third party until the sale is complete.
When the value of property declines.
Discount points (or Points)
Money paid to a lender at closing in exchange for lower interest rates. Each point is equal to 1 percent of the loan amount.
Down payment
Money paid for a house from one's own funds at closing. The down payment will be the difference between the purchase price and mortgage amount.
Earnest money
Deposit made by a buyer in evidence of good faith when the purchase agreement is signed.
Equal Credit Opportunity Act (ECOA)
Federal law requiring creditors to make credit equally available without discrimination based on race, color, religion, national origin, age, sex, marital status, or receipt of income from public assistance programs.
The percentage of property value held by the owner; the difference between the current market value of a property and the outstanding mortgage balance.
Equity loan
A loan based on the borrower's equity in his home.
The neutral third party that holds money and/or documents until the escrow instructions are fulfilled and escrow can be a title company or an attorney, depending on state regulations.
Escrow account
Account held by a lender containing funds collected as part of mortgage payments for annual expenses such as taxes and insurance, so that the homeowner does not have to pay a large sum when these fall due.
Escrow waiver
Escrow Waiver is waiver of the requirement to fund an escrow account with lender and instead pay insurance and taxes separately. This waiver may require a fee and is not available with all loan programs.
Fair Housing Act
Prohibits discrimination in real estate transactions because of race, color, religion, sex, handicap, familial status (families with children), or national origin. It applies to mortgage lending as well as other aspects of real estate transactions, including sales and rentals, real estate brokerage, and appraisals.
Farmer's Home Administration (FMHA)
An agency within the U.S. Department of Agriculture that provides financing for homes and farms in small towns and rural areas.
Federal Home Loan Mortgage Corporation (FHLMC or Freddie Mac)
Quasi-governmental agency that purchases conventional mortgages from insured depository institutions and HUD-approved mortgage bankers.
Federal Housing Administration (FHA)
A government agency, division of the Department of Housing and Urban Development, that insures residential mortgage loans made by private lenders and sets standards for underwriting mortgage loans.
Federal National Mortgage Association (FNMA or Fannie Mae)
A quasi government agency created by Congress that buys and sells residential loans.
Federal Reserve
The central bank of the United States and major regulatory agency for many commercial banks.
Fee simple
Absolute ownership of real property.
First mortgage
A mortgage that is in first lien position, taking priority over all other liens. In the case of foreclosure, the first mortgage will be repaid before any other mortgages.
Fixed rate
An interest rate that is fixed for the term of the loan.
Fixed-rate mortgage
A mortgage with an interest rate that doesn't change for the life of the loan, guaranteeing fixed payments.
Flood insurance
A form of hazard insurance required by lenders to cover properties in flood zones.
Foreclosure (or repossession)
Legal process by which the lender forces the sale of a property because the borrower has not met the mortgage terms.
Government National Mortgage Association (GNMA or Ginnie Mae)
A government agency that provides funds for VA and FHA loans.
Graduated Payment Mortgage (GPM)
A mortgage with initial low payments (with potential negative amortization) that increase regularly for several years and then level off.
Gross income
Total income before taxes or expenses are deducted.
Hazard insurance
Protects the insured against loss due to fire or other natural disaster in exchange for a premium paid to the insurer.
Home equity loan
A loan secured by equity in a property. These are sought for a variety of purposes, including home improvements, major purchases or expenses and debt consolidation.
Homeowners warranty
A type of insurance that covers repairs to specified parts of a house for a specific period of time.
Housing and Urban Development (HUD)
A U.S. government agency established to implement federal housing and community development programs; oversees the Federal Housing Administration.
Initial rate
The rate charged during the first interval of an ARM.
Charge paid for borrowing money, calculated as a percentage of the amount borrowed.
Interest rate
The periodic charge, expressed as a percentage, for use of credit.
Interest rate cap
A safeguard built into ARMs to prevent drastic changes in interest rates.
Joint liability
Liability shared among two or more people, each of whom is liable for the full debt.
Joint tenancy
The ownership of property by two or more persons with the survivor taking the share of the deceased.
Jumbo loan
A mortgage larger than the limits set by the Federal National Mortgage Association and the Federal Home Loan Mortgage Corporation. Because jumbo loans cannot be funded by these two agencies, they usually carry a higher interest rate.
The bank, mortgage company or mortgage broker offering a loan.
A claim by one person on the property of another for payment of a debt.
Loan estimate
An estimate of all closing fees including pre-paid and escrow items as well as lender charges. It must be given to the borrower within three days after submission of a loan application.
Loan origination fee
A fee a lender charges to process a mortgage, usually expressed as a percentage of the loan (or points), which pays for the work in evaluating and processing the loan.
Loan to value ratio (LTV)
The percentage of the property value borrowed. (Loan amount/property value=LTV)
Lock or lock-in
A lender's guarantee of an interest rate for a set period of time, usually between loan application and loan closing. This protects borrowers against rate increases during that time.
The number of percentage points added to an index to calculate the interest rate on an ARM at each adjustment.
Marketable title
A title free and clear of liens, clouds or other defects that would prevent the sale of the property.
A document that creates a lien on a property as security for the payment of a debt.
MIP (Mortgage insurance premium)
Insurance purchased by borrower to insure against default on a FHA loans.
Mortgage loan
A loan for which real estate serves as collateral to provide for repayment in case of default.
Mortgage note
A legal document that obligates a borrower to repay a loan at a stated interest rate during a specified period of time. The agreement is secured by a mortgage.
Non-conforming loan
A conventional loan that cannot be sold to Fannie and Freddie Mac. Often, these loans are larger than the conforming loan amount.
Non-dischargeable debt
Debt, such as taxes, that cannot be forgiven in a bankruptcy liquidation.
Legal document stating the terms of a debt and a promise to repay it.
Notice of default
Written notice to a borrower that a default has occurred and that legal action may be taken.
Payment cap
Limit on the amount by which a borrower's ARM payments may increase, regardless of rise in interest rates. This may result in negative amortization.
Payment cap (ARM)
A pre-determined amount that establishes the maximum by which the payment can increase, irrespective of increases to the interest rate.
Payment change date
Dates upon which the payment amount is subject to change. Products featuring "negative amortization" typically will include a payment change date which differs from the interest rate change date in frequency.
Permanent loan
A long-term mortgage of 10 years or more.
Piggyback mortgage
A combination of a first mortgage for 80% of property value, and a second for 5%, 10%, 15%, or 20% of value. These combinations are designated as 80/5/15, 80/10/10, 80/15/5, and 80/20/0, respectively. Piggybacks are a substitute for mortgage insurance for borrowers who cannot put 20% down.
Also called "monthly housing expenses," principal, interest, taxes and insurance are the components of a monthly mortgage payment.
A full or partial payment of the principal before the due date. This might occur if the borrower makes extra payments, sells the property or refinances the existing loan.
Pre-payment penalty
Some ARM loans contain a provision against pre-payment without penalty. Terms of pre-payment penalty clauses vary from product to product, investor to investor, and state to state. Many states and even local municipalities have, or are contemplating, enacting legislation against pre-payment penalties.
The process of determining how much money a prospective homebuyer may borrow, prior to application for a loan.
The amount of debt, not counting interest, left on a loan.
Private Mortgage Insurance (PMI)
Insurance purchased by a buyer on a conventional loan when a down payment is less than 20 percent of the purchase price to protect the lender against default.
Profit and loss statement
A financial statement showing revenue, expenses and profits over a period of time.
Property tax
A government tax based on the market value of a property.
Purchase agreement
A contract signed by buyer and seller stating the terms and conditions of a home sale.
Real Estate Agent
A real estate professional who is a member of the National Association of Realtors.
Real estate broker
An agent representing a buyer or seller in a real estate transaction.
The process of paying off one loan with the proceeds from a new loan secured by the same property.
The cancellation of a contract, permitted by law within three business days of signing a mortgage not used to purchase a home.
Secondary mortgage market
The market into which primary mortgage lenders sell the mortgages they make to obtain funds to originate more new loans. This includes investors such as Fannie Mae and Freddie Mac.
Second mortgage
A subordinate mortgage made in addition to a first mortgage.
Settlement (or Closing)
A meeting between the buyer, seller and lender (or their agents) where property and funds legally change hands.
Settlement cost (HUD guide)
A booklet given to consumers after applying for a loan that provides an overview of the lending process.
A measurement of land, prepared by a licensed surveyor, showing a property's boundaries, elevations, improvements and relationship to surrounding tracts.
Tax lien
Claim against a property for unpaid taxes.
The number of years until a loan is due to be paid in full.
A document that gives evidence of ownership of a property, as well as rights of ownership and possession.
Title company
A company that insures the title to a property.
Title insurance
Insurance that protects the lender (lender's policy) or buyer (owner's policy) against loss due to disputes over property ownership.
Title search
Examination of municipal records to ensure that the seller is the legal owner of a property and that there are no liens other claims against the property.
Someone given legal responsibility to hold property in the best interest of another.
Truth-in-Lending Act (TIL)
A federal law requiring written disclosure of the terms of a mortgage (including APR and other charges) by a lender to a borrower after application.
The process of verifying data and evaluating a loan application. The underwriter gives the final loan approval.
VA Loan
A home loan available to veterans with little or no down payment and guaranteed by the U.S. Veterans' Administration.
Verification of deposit (VOD)
A document signed by the borrower's bank or other financial institution that verifies the borrower's account balance and history.
Verification of employment (VOE)
A document signed by the borrower's employer that verifies the borrower's position and salary.
The form you get from your employer every year and used for filing your income tax returns.
Loan Options Mortgage Calculators Contact Us


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The debut EP from Mexicans In Obscurity Revealed is out in but a month's time on Blood Harvest Records, and it is a bleak, nihilistic slab of twisted decay. If this is a precursor to their upcoming full length then count me in, because 'Grim Fumes of Revelation' is excellent.
The burning hatred that fans the flames of opener 'Storms Conjured' blinds like the noonday sun, with scathing riffage slicing through flesh and bone. In Obscurity Revealed are raw, but not incomprehensible. Their material is more of the surgeon's knife than the frenzied bludgeoning of some black/death metallers. But that knife is coated in disease, leading to the atonal melodies that spiral around the main, barbed riff.
'Varcolaci' continues this path, with an opening riff that is as icy cold as anything to come out of Norway 20 years ago, but leading into the twisted offspring of Marduk and Deathspell Omega. Black metal is no longer one dimensional, and these new bands breathe new, fetid life into the black and white corpse that old school black metal has become. By injecting glorious, raging energy into the genre again, In Obscurity Revealed show that you don't have to buck the blueprint a lot, but if its executed well, it is a fucking delight. 'Grim Fumes of Revelation' is that delight, now spill blood in the name of GRIMNESS!


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+1 (702) 466-1229Open 24 Hours a day 7 days a week
The secrets of the Far East will be revealed tonight when you have me by your side. Right now as you look at my photographs think about this…If you call me right now and invite me over. I am alone, waiting, and in the mood to play. My games are a whole lot of fun and will leave you smiling and exhausted but with a pleasant lifetime memory of your visit to the City of Sin.
How many hours do you have free this evening? I'm available all night long and can even stay a few days if you want me to. We can have lots of fun both indoors and out. I love to strip in the privacy of your room. I'm also a great companion and conversationalist and know my way around town if you want to spend some time seeing a show or going to the casinos. I'm here right now, alone, and free for you to snatch up for the night. Call me.
Disclaimer: Money exchanged for outcall entertainment services is for Azumi's time and companionship only 😍.


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The CEPA Strategy and Action Plan (2019–2024) was adopted at the MOP10 and aims to provide the communication and education tools (skills, templates, materials etc.) to raise awareness of the importance of the EAAF so that people will participate in activities that contribute towards the conservation of migratory waterbirds and their habitat that will benefit the community and contribute to sustainable development.
The key actors for implementation of this CEPA strategy include those working at the Flyway, national and sites level. These include governments, site managers, multilateral environment agreements, technical and academic institutions, development agencies, private sector groups, non-governmental organisations and local communities.
The Secretariat encourages Partner countries to translate the CEPA Strategy and Action Plan into their languages.
Partnership Communication Strategy document
These files are in pdf format. Download the Adobe Acrobat reader.
Flags indicate document language


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Do You Suffer From Joint Pain, Knee or Back Pain?
Stem cell injection therapy may be exactly what you've been searching for.
What Is Stem Cell Injection Therapy?
Stem Cell Therapy is a non-surgical solution for joint, knee, and back pain. The simple in-office procedure helps initiate the body's self-recovery process allowing patients to quickly get back to their normal routine.
Stem cell injections have shown promising results for men and women with chronic disorders who aren't ready to undergo risky surgical procedures. Treatments safely and effectively provide long-term results.
How Does It Work?
Stem Cell Therapy uses high-concentrations of living tissue to repair damaged cells within the body. When injected directly into predetermined problem areas, stem cells can facilitate a faster recovery process sans surgery. Treatments are quick, easy, and can typically be done in less than an hour.
What Areas of the Body Does It Treat?
Undifferentiated stem cells have the ability to grow into virtually any type of cell in the body making them effective for a variety of conditions. When injected at precise locations, the cells start to take instructions from surrounding cells and eventually duplicate them. Stem cells can be beneficial for;
- Joint Pain
- Knee Pain
- Back Pain
When treating joint disorders or knee pain, stem cells are placed in areas where they will develop into essential cartilage and meniscus cells. For back pain, stem cells are injected on either side of the spine in either the lower back or neck regions where they'll grow into new spinal disks, tendons, or muscle tissue.
Who Is A Good Candidate for Stem Cell Therapy?
You may be a good candidate for Stem Cell Therapy if you'd like to successfully avoid more invasive surgical options for back or knee pain caused by past trauma or injury. Stem Cell Therapy is also effective for treating age or genetic-related joint pain. Dr. Lester will determine your candidacy for the procedure at the time of your consultation.
How Many Treatments Are Needed to See Results?
In many cases, the anti-inflammatory effects of stem cell injections are noticed within days. Patients will often walk better immediately after injection into the knees. It takes 9-12 weeks for new tissue to start to grow. Repeated injections at 3-6 month intervals are needed when there is more extensive damage, or if a person is ill or elderly.
Is It Painful?
Aside from minor pain at the injection site, Stem Cell Therapy is typically well tolerated. A topical anesthetic cream is applied beforehand, and injections have anti-inflammatory properties to minimize any post-treatment discomfort.
Is There A Recovery Process?
There is no typically downtime after the injection or infusion. Depending on the significance of your injury, Dr. Lester may create a custom recovery plan.
Where Do Stem Cells Come From?
At Trilogy Medical, we use FDA registered and inspected stem cells that have been prepared by the company RichGen. These stem cells are derived from a young healthy woman's placenta after a C-section birth. Because cells are purified and isolated for injection therapy, they contain no DNA remnants of the baby or mother.
Stem cells that are sourced from amniotic fluid are much more effective than cells that come from your bone marrow or fat cells because they are undifferentiated. Undifferentiated cells are more likely to respond and grow into the healthy tissue your body instructs them to.
Take The Next Step
Interested in learning more about Stem Cell Injection Therapy? Schedule your consultation with Trilogy Medical & Aesthetics today by filling out the form on the side of this page or by calling one of our three practice locations in Campbell (408) 844-0010, Santa Cruz (831) 600-8117, or Watsonville (831) 724-1164.
*Individual Results May Vary


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The Bees treat every customer so special, they'll think it's their birthday with each interaction!
Carrie Jones
President /
A graphic designer and production artist, Carrie graduated in 1999 from The Creative Circus in Atlanta to begin her career in marketing and communications. She has served a long list of agencies and organizations as a studio artist, graphic designer and freelancer, collaborating with clients large and small to design, polish and produce key print communication pieces. Carrie founded The Hive Solution in 2014.
Carrie takes a great deal of pride in professionalism — that includes understanding client needs, getting the job done quickly and meeting deadlines. As a designer and marketing specialist, she is not only buzzing with creativity, clients describe her as detail-oriented, disciplined and well-organized.
Nina Peace
Relational Account Manager /
Nectar Director
Nina has 20 years of experience in Customer Service roles, and an extensive background in education and leadership. Before joining The Hive in 2017, she worked as a Program Director in partnership with her local Department of Education to manage programs for improving teacher and parent relationships.
Nina is passionate about building relationships with strong communications. She holds professional certifications in Diversity and Management, is a committed volunteer working with veterans and special needs adults, and loves spending time with her sons.
Anthony Wiley
Relational Account Manager /
Bearded Bee
Anthony has a degree in Business Administration with a concentration in Marketing from Indiana University. He has extensive experience in corporate and government business development, as well as collaborating and consulting with various levels of management. Anthony is a resourceful, goal exceeding team player with the ability to manage his workload successfully while implementing organizational strategies.
Anthony specializes in business partnership development as well as operations and process improvement. He is a skilled project manager with a talent for strategic planning and problem solving. During his down time, Anthony enjoys quiet time fishing.


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Westend MasonThese Westend Mason are fun, oversized oval frames with a slight cat eye browline. Feel sophisticated and classy in these unique frames.
- Brand authenticity guaranteed
- Westend logo on temple
- Spring hinges
- Branded eyeglass case included
- Age Range: Adult
- Frame Shape: Cat Eye
- Frame Type: Full Frame
- Frame Material: Plastic
- Brand: Westend
- Frame Weight: Ultralight
Frame Size
Have a Frame That Fits?
Frame measurements may have slight differences depending on the options selected above.
with lenses*


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Bus Driver at Palo Alto Unified School District
Job Information
Job Summary
Job Summary
nder supervision, to operate a school bus over designated routes to transport school children; and to perform related work as required. Specific Duties Include: • Operate a school bus daily over designated routes in accordance with time schedules • Pick up and discharge school children safely according to transportation rules • Escort children across street, stopping traffic when necessary • Transport students and teachers on field trips to various locations, choosing the best route and making departure and arrival time as scheduled • Service bus with gas and oil and check tires and battery • Wash bus exterior and clean interior and assist in maintaining bus in safe operating condition • Maintain good order among students on the bus • Follow district policies regarding the disciplining of children and contact with parents and other citizens • Keep record of mileage, fuel and oil, and prepares reports of driving hazards and incident • Other duties as assigned.
Requirements / Qualifications
Requirements / Qualifications


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Experimental Electronics And Other Music
Showcasing Interesting Music. No illegal downloads.
Fernando Wax
from soundcloud:
Broadcast on October 11rd at 20:00 on Radio Vibration (vibration.fm) in Brussels, Belgium. DJ Set by Fernando Wax. This is a part of the set that I had the privilege to do at Neon Judgement's last concert After Party which took place in Brussels on September 26th.
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2011 Christmas Letter … the wait is over
Twas the Rowan Letter of Christmas, when all through Mark's mind not an idea was stirring, not of any kind. The paper was blank as was Mark's stare, in hopes that a decent idea soon would be there.
The children were jumping on their beds, while trying to punch each other in their heads. And mamma in her 'kerchief, and I in my cap … juuust kidding I'm not doing this. And what the what is a kerchief? Anybody .. anybody???
I hope you are ready to enjoy this holiday season, since the world ends next year. Thanks a lot, Mayans. Drink lots of eggnog and eat loads of figgy pudding (another Christmas mystery) because the aliens are going to horde it all.
Well, it's no mystery that I have the best family in the world. I looked it up on Wikipedia to confirm and Jenny is the number one wife and mother of all time. Right on schedule she birthed our fourth child in seven years. Now that is production, folks, or REproduction. God's says multiply and we say yes sir. Jenny has the most rewarding/difficult job known to mankind and she does it marvelously. Keep it up, all you moms. We wouldn't be here without you, literally and figuratively.
Elena Kay has been sweeping in the awards in 1st grade. It took her about 3.8 seconds to win Citizen of the Month in September and in November she was the Holland Husky Hero. No, she hasn't gained a lot of weight. Husky is the mascot. It does mean she was the best behaved. A trait she obviously inherited from her father. She is into reading books (I told her its overrated, but she continues to learn to read.) and her teacher Mrs. Dozier loves her the mostest. (She didn't say that, but I could deduce as much from the parent/teacher conference. A parent knows these things.)
Cassia is busy learning the finer things of education in pre-school. Her teacher is sooooo hawt. One of the endearing aspects of Cassia is her love for ugly things. That's why she likes me so much!!! I had to say it before you thought it. She will always pick out the strangest/weirdest toy. She has a heart for the downtrodden, meaning she is predestined to be a Redskins fan. Cassia is the most quotable of the bunch, i.e. a recent exchange between her and Elena Kay … EK: Get away! C: Never! I'm your sister!!!
Josiah. What can I say? He pees in the potty and poops in his pants. He makes us laugh constantly. Although, we're usually not laughing after a pooping in the pants episode. Sounds funny, but it's not. His Tai Kwan Do skills are quite impressive for an almost 3 year old. He has no formal training, but he has a God-given proclivity to kick and punch things (which may or may not be his sisters). Despite his fighting prowess, he is the quickest to give hugs and kisses to anyone within arms reach.
Adalyn arrived July 19th and our mantra has been "4, no more!" She rocks a fo-hawk like it ain't no thang and likes to tell us all about her day in the middle of the night sometimes. She has no lack for attention, and it is plain to see where the term "babied" comes from. Sometimes the babying annoys the snot out of her when it is coming from her older siblings, though. She has dimples −− a Rowan kid first and she is my sweet Lil Pee Peeps.
I surely do love some Christmas. The whole season is good for the soul. Mostly because it's a reminder of what is best for the soul. Giving, sharing, spending time with loved ones are all wonderful traditions of the season, but it is the recollection that Jesus was sent to the earth to redeem our souls that is a true wonder. I always like to end on a serious note, but in reality its the most joyful news I can share about our family. Jesus is the center of it all and without him Christmas would be a real drag. And it would just be called Mas
… not very catchy. We love you. Have the best 2012 ever!
Love … The Rowans


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I love when I get home and discover I have leftover rice, because that translates to dinner in under 20 minutes. This happened to me some 2 weeks ago and boy was I happy.
I had a feeling I had some sausages in the freezer and lucky me, I spotted the last three. I also had some peas that I had boiled and stored in the fridge. The beauty of boiling peas prior is that when it comes to the actual cooking all you'll need to do is thaw them then cook as desired.
This dish is similar to the egg fried rice I made sometime back sans the eggs.
1 onion chopped
1 cup of pre cooked peas thawed
3 sausages fried and diced
1/2 bell pepper (hoho) cubed
Leftover rice
Salt and pepper to taste
2-3 tbsps of vegetable oil for frying
In a skillet add the vegetable oil then fry the onions till tender.
Add the bell peppers.
Add the rice and peas into the skillet.
You just need to get them warmed up, since they are already cooked.
Finally add in the sausages.
Dinner is served.


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The gram-negative, facultative intracellular bacterium Francisella tularensis causes acute, lethal pneumonic disease following infection with only 10 CFU. The mechanisms used by the bacterium to accomplish this in humans are unknown. Here, we demonstrate that virulent, type A F. tularensis strain Schu S4 efficiently infects and replicates in human myeloid dendritic cells (DCs). Despite exponential replication over time, Schu S4 failed to stimulate transforming growth factor β, interleukin-10 (IL-10), IL-6, IL-1β, IL-12, tumor necrosis factor alpha, alpha interferon (IFN-α), and IFN-β throughout the course of infection. Schu S4 also suppressed the ability of directly infected DCs to respond to different Toll-like receptor agonists. Furthermore, we also observed functional inhibition of uninfected bystander cells. This inhibition was mediated, in part, by a heat-stable bacterial component. Lipopolysaccharide (LPS) from Schu S4 was present in Schu S4-conditioned medium. However, Schu S4 LPS was weakly inflammatory and failed to induce suppression of DCs at concentrations below 10 μg/ml, and depletion of Schu S4 LPS did not significantly alleviate the inhibitory effect of Schu S4-conditioned medium in uninfected human DCs. Together, these data show that type A F. tularensis interferes with the ability of a central cell type of the immune system, DCs, to alert the host of infection both intra- and extracellularly. This suggests that immune dysregulation by F. tularensis operates on a broader and more comprehensive scale than previously appreciated.
Francisella tularensis is a gram-negative, facultative intracellular bacterium and the causative agent of tularemia. Although the bacteria was identified nearly 100 years ago, the nature of its interaction with host cells and tissues has remained largely undefined until recent times. The unfortunate realization of the potential of F. tularensis as a biological weapon has resulted in a resurgence of research on tularemia. Much of our recent understanding of tularemia pathogenesis has come from manipulation of the mouse model of Francisella infections. While these murine studies have yielded many important advances in our understanding of tularemia pathogenesis, very little is understood about how Francisella, especially the most virulent type A strains such as Schu S4, interacts with human cells.
Dendritic cells (DCs) serve as a central cell type in the immune system, bridging the innate and adaptive immune response to effectively eradicate invading pathogens. Thus, it is unsurprising that many microbes have developed mechanisms by which to modulate these cells to evade host immune responses (4, 30). F. tularensis is no exception in its ability to modify DC responsiveness to infection. For example, in the mouse model, both attenuated and virulent strains of F. tularensis fail to induce the production of cytokines required for mobilization of key effector cells (7, 8, 14, 50). However, only virulent F. tularensis also prevents increased expression of key surface receptors required for antigen presentation in the lung in vivo (7). It is not known if virulent F. tularensis has the same effect on human DCs in vitro.
A few recently published studies have focused on the attenuated F. tularensis live vaccine strain, LVS, and F. tularensis subsp. novicida in human cells. However, both of these subspecies are attenuated in humans. Due to this attenuation, it is unsurprising that following infection with these strains, human DCs and monocytes are activated to produce proinflammatory cytokines and upregulate receptors associated with antigen presentation and that DCs can easily control bacterial replication when exposed to the appropriate stimulus following infection (22, 26, 27, 31). However, this does not necessarily reflect how human cells, in particular DCs, might behave when infected with a more formidable and virulent strain of F. tularensis.
Here, we provide data supporting our hypothesis that, unlike more attenuated Francisella species and despite exponential replication, type A F. tularensis fails to induce production of both proinflammatory and anti-inflammatory cytokines by human DCs. As observed in the murine model, this suppression of cytokine secretion mediated by F. tularensis was an active process requiring live organisms for optimal effect. Furthermore, we made the surprising observation that F. tularensis also inhibited responsiveness of uninfected bystander DCs. At high concentrations (100-fold greater than Escherichia coli lipopolysaccharide [LPS]), purified LPS from F. tularensis strain Schu S4 was capable of inducing minimal endotoxin tolerance to E. coli LPS. However, our data suggest that Schu S4 LPS present in tissue culture medium was not the primary mediator of the suppression observed in human DCs. Rather, an undefined, moderately heat-stable molecule shed or secreted by Schu S4 significantly inhibited human DC responsiveness to secondary stimuli. Furthermore, our evidence suggests that modulation of DCs by Schu S4 components in the extracellular space is different from that observed among infected cells. Together, these results correlate with our in vivo observation that Schu S4 potently suppresses cells critical for initiation of innate immunity. Data presented herein also represent an important step forward in understanding how virulent F. tularensis manipulates the human host and provides a novel mechanism by which this bacterium successfully suppresses host cells in a global sense.
Bacteria and bacterial products. F. tularensis strain Schu S4 was kindly provided by Jeannine Peterson (Centers for Disease Control, Fort Collins, CO). Green fluorescent protein (GFP)-expressing Schu S4 was generated as previously described (12). Schu S4 was cultured in modified Mueller-Hinton broth ([MMH] Mueller-Hinton broth supplemented with CaCl2, MgCl, 0.1% glucose, 0.025% ferric pyrophosphate and 2% Isovitalex) at 37°C with constant shaking overnight, aliquoted into 1-ml samples, frozen at −80°C, and thawed just prior to use, as previously described (7). Titers were determined in frozen stocks by enumerating viable bacteria from serial dilutions plated on MMH agar as previously described (9, 19). The number of viable bacteria in frozen stock vials varied less than 5% over a 10-month period.
Killed Schu S4 was generated by resuspending 1 ml of 2 × 109 CFU/ml Schu S4 in 1% paraformaldehyde. Following overnight incubation at 4°C, bacteria were washed three times in phosphate-buffered saline (PBS), resuspended in 1 ml of PBS, and stored at 4°C. Killed Schu S4 was detected via intracellular staining with AlexaFluor 647-labeled anti-F. tularensis LPS(anti-LPSFt) antibody (US Biological, Swampscott, MA). Isotype control antibody (R&D Systems) labeled with AlexaFluor 647 served as a negative control for the presence of killed Schu S4. Anti-LPSFt and isotype antibodies were labeled using an AlexaFluor 647 monoclonal labeling kit (Invitrogen) according to manufacturer's instructions.
Schu S4-conditioned medium (S4CM) was generated following incubation of 107 CFU of F. tularensis Schu S4 overnight in RPMI medium supplemented with 10% heat-inactivated fetal calf serum, 0.2 mM l-glutamine, 1 mM HEPES buffer, and 0.1 mM nonessential amino acids (all from Invitrogen) (complete RPMI [cRPMI] medium) at 37°C in 7% CO2. Cultures were collected and filter sterilized through a 0.2-μm-pore-size syringe filter. As indicated, some aliquots of S4CM were heated at 95°C for 1 h [S4CM(95C)]. F. tularensis Schu S4 LPS was generated as previously described (10, 15). Ultrapure E. coli LPS was purchased from InvivoGen (San Diego, CA).
Generation of human DCs.Human myeloid DCs were differentiated from peripheral blood monocytes that had been subjected to apheresis as previously described (6, 42). Briefly, monocytes that had been subjected to apheresis were enriched using Ficoll-Paque (GE Healthcare). CD14+ progenitor cells were enriched via negative selection using a Dynabeads MyPure Monocytes Kit for untouched human cells, per the manufacturer's instructions (Invitrogen). Cells were resuspended at 5 × 105/ml in cRPMI medium supplemented with 100 ng/ml granulocyte-macrophage colony-stimulating factor and 20 ng/ml interleukin-4 (IL-4) (both from Peprotech), plated at 2 ml/well in six-well plates, and incubated at 37°C in 5% CO2. On day 2 of culture, 0.5 ml of medium was removed and replenished with 1 ml of cRPMI medium supplemented with 100% cytokines. All cells were used on day 4 of culture. The resulting differentiated DCs were >97% CD1a+/DC-specific intercellular adhesion molecule-grabbing nonintegrin (DC-SIGN)-positive and <1% CD14−. Human blood cells were collected from anonymous volunteers under a protocol reviewed and approved by the NIH Institutional Biosafety Committee.
Infection, bacterial enumeration, and stimulation of DCs.DCs were infected at a multiplicity of infection (MOI) of 50 with F. tularensis strain Schu S4. DCs were removed from their original cultures and pelleted. The resulting DC-conditioned medium was reserved for replating of cells. DC numbers were adjusted to 2 × 107 to 3 × 107/ml in reserved DC medium. Cells treated with medium alone served as negative controls. Schu S4 was added, and cells were incubated at 37°C in 7% CO2 for 1 h, washed once, and then incubated with 50 μg/ml gentamicin (Invitrogen) for 45 min to kill extracellular bacteria. Then, cells were washed extensively and adjusted to 5 × 105 cells/ml in reserved DC medium and then plated at 1 ml/well in 24-well tissue culture plates. As indicated, 10 μg/ml of anti-IL-10, anti-pan transforming growth factor β (TGF-β), or the appropriate isotype control (all from R&D Systems) was added to each well immediately after infection of DCs. In additional experiments, 4 μg/ml gentamicin was added 12 h prior to stimulation of DCs with Toll-like receptor (TLR) agonists. This concentration has been previously shown to be the MIC for control of F. tularensis replication (3). In these experiments, immediately prior to the addition of TLR agonist, an aliquot of the medium was collected, serially diluted, and plated onto MMH agar to enumerate extracellular bacteria. At the indicated time points, ultrapure LPS (TLR4 agonist), zymosan (TLR2 and C-type lectin agonist), or tripalmitoyl-Cys-Ser-(Lys)4 (Pam3CSK4; a TLR2 agonist) (10 ng/ml, 10 μg/ml, and 1 μg/ml, respectively) (InvivoGen) was added to the appropriate wells. Cultures were incubated for 24 to 72 h at 37°C in 7% CO2. Supernatants were collected at each time point and stored at −80°C. To determine uptake and replication of bacteria, DCs were harvested from each well, pelleted at 1,200 rpm for 5 min, and incubated with 50 μg/ml gentamicin for 45 min at 37°C in 7% CO2. Cells were then washed extensively and lysed following incubation in water for 5 min. The last wash from each sample was plated onto MMH agar to confirm depletion of residual extracellular bacteria. There were no bacteria detected in these samples in each experiment tested. Cell lysates were serially diluted, plated onto MMH agar plates, and incubated at 37°C in 7% CO2 for approximately 48 h and individual colonies were enumerated. Replication of GFP-Schu S4 was also analyzed by flow cytometry (described below).
As indicated, uninfected DCs were resuspended in S4CM or S4CM(C95). DCs were incubated overnight, followed by addition of ultrapure LPS as described above. DCs were then stained for intracellular cytokines as described below.
Experimental and control groups were all performed in triplicate. The standard error of the mean (SEM) and statistical significance between treatment groups were determined by analysis of variance, followed by Tukey-Kramer's comparison of means.
Depletion of Schu S4 LPS from S4CM.Schu S4 LPS was depleted from S4CM using anti-LPSFtantibodies (US Biological). Briefly, S4CM was incubated with 5 μg/ml anti-LPSFtantibodies or anti-mouse immunoglobulin G2a (IgG2a) as an isotype control for 1 h at 4°C with constant rotation. To remove antigen/antibody complexes, magnetic beads bound with anti-mouse IgG antibodies (Invitrogen) were added to treated S4CM and allowed to incubate for 1 h at 4°C with constant rotation. Samples were then placed on a Dynal MPC-50 magnet (Invitrogen) to immobilize complexed beads, and the resulting supernatant was collected. Depletion of Schu S4 LPS from S4CM was monitored by Western blotting and enzyme-linked immunosorbent assays (ELISAs) (described below). The indicated samples were prepared per manufacturer's instructions and were first resolved on a 12% Bis-Tris sodium dodecyl sulfate-polyacrylamide gel electrophoresis gel, followed by blotting onto polyvinylidene difluoride using XCell Mini Cell and XCell II Blot modules (Invitrogen). Blots were blocked with 5% nonfat milk in Tris-buffered saline plus Tween 20 (TBST), washed, and then incubated with anti-LPSFtantibody (US Biological) diluted 1:200 in TBST. Blots were washed and incubated with horseradish peroxidase (HRP)-conjugated anti-mouse IgG to detect primary antibody bound to the membrane. Blots were washed again and incubated with SuperSignal West Pico Chemiluminescent Substrate (Pierce, Rockford, IL) to detect HRP. HRP activity was detected using a Kodak 4000MM imager and Kodak MI software (Kodak).
Schu S4 LPS ELISA.Quantification of Schu S4 LPS in S4CM was performed by ELISA. Briefly, Schu S4 LPS was coated onto Immunlon 2HB plates in 0.1 mm sodium bicarbonate buffer overnight at 4°C. Plates were washed with PBS-0.2% Tween 20, and samples were added. A standard curve was generated by serially diluting purified Schu S4 LPS and adding it to the plate. Plates were incubated for 1 h at room temperature and washed as above. Mouse anti-Francisella LPS antibody (US Biological) was added, and plates were incubated for 1 h at room temperature. Plates were washed, incubated with HRP-conjugated donkey anti-mouse antibody (Jackson ImmunoResearch), and washed again. Bound antibody was detected following addition of 1-Step ABTS [2,2′-azinobis(3-ethylbenzthiazolinesulfonic acid)] (Pierce) and analysis of absorption at 450 nm using a Dynex MRX Revelation instrument and Revelation software (Dynex Technologies, Chantilly, VA).
Flow cytometry and intracellular staining.GFP-Schu S4 and intracellular cytokines were detected by flow cytometry as previously described (21). At the indicated time points in each figure and 1 h after addition of ultrapure LPS (10 ng/ml), zymosan (10 μg/ml) or Pam3CSK4 (1 μg/ml) and 5 μg/ml brefeldin A (BFA; Invitrogen) was added to DC cultures. Cells were then incubated at 37°C in 7% CO2 for 5 h. After incubation, cells were washed once and resuspended in Flow Cytometry Staining buffer (fluorescence-activated cell sorter [FACS] buffer; eBioscience). Then, cells were fixed in 2% paraformaldehyde in PBS for 10 min at 37°C in 7% CO2 and washed twice more in Perm buffer (FACS buffer supplemented with 0.25% saponin [Sigma-Aldrich]). Next, cells were incubated at room temperature with anti-human tumor necrosis factor alpha (TNF-α) (phycoerythrin [PE]conjugated; clone Mab11), anti-human IL-12/IL-23p40/70 (PE coupled; clone C8.6) or mouse IgG1 (PE coupled) as an isotype control (all from eBioscience). Cells were incubated with cytokine or isotype control antibodies for 20 min at room temperature. Cells were washed twice in Perm buffer, fixed in 1% paraformaldehyde for 30 min, and then resuspended in FACS buffer at 4°C until analysis. Cells were acquired and analyzed using a CyFlow ML flow cytometer and FlowMax software (Partec).
Detection of secreted cytokines.Culture supernatants were assayed for the presence of TNF-α, IL-6, IL-10, IL-1β, IL-12/IL-23p40, TGF-β, alpha interferon (IFN-α), and IFN-β by ELISA using commercially available kits according to the manufacturer's instructions (R&D Systems and PBL Interferon Source).
Fluorescence microscopy.DCs were infected with GFP-Schu S4 as described above and then adhered to a glass slide using a Shandon Cytospin 4. Cells were fixed in 3% paraformaldehyde for 30 min at 37°C in 5% CO2. Cells were washed with PBS and stained for cleaved caspase-3 using rabbit anti-cleaved caspase-3 antibody (Cell Signal Technology) and then AlexaFluor 568 anti-rabbit IgG, following the manufacturer's instructions exactly. Samples were visualized using a Carl Zeiss LSM 510 confocal scanning laser microscope for quantitative analysis and image acquisition. Confocal images of 1,024 by 1,024 pixels were acquired and assembled using Adobe Photoshop CS2 software (Adobe Systems, San Jose, CA).
Statistical analysis.Statistical differences between two groups were determined using an unpaired t test with the significance set at a P value of <0.05. For comparison between three or more groups, analysis was done by one-way analysis of variance followed by Tukey's multiple comparisons test with significance determined at a P value of <0.05.
Schu S4 infects and replicates in human DCs.As a facultative intracellular pathogen, F. tularensis Schu S4 can replicate in both the intra- and extracellular environments. We along with others have shown that more attenuated LVS replicates exponentially in both mouse and human DCs (5, 8). However, the efficiency of Schu S4 replication in human myeloid DCs has not been described. Since infection and intracellular replication are likely to be an integral element of Schu S4 pathogenesis, we first determined if human DCs were permissive to uptake and growth of Schu S4. Schu S4 was readily taken up by DCs and replicated intracellularly exponentially over time in human DCs (Fig. 1A). Due to the low numbers of bacteria recovered from the earliest time point, it was unlikely that all DCs in the cultures were infected. To monitor the number of cells infected at any given time, we also infected DCs with GFP-expressing Schu S4 (GFP-Schu S4) and analyzed DCs by flow cytometry. Corresponding with recovery of low numbers of viable Schu S4 from DC lysates, only about 5% of DCs were positive for GFP-Schu S4 24 h after infection. In correlation with exponential intracellular replication observed in cell lysates, by 48 h 20 to 25% of cells were positive for GFP-Schu S4, and by 72 h after infection nearly all DCs (>80%) were positive for GFP-Schu S4 (Fig. 1B and C). GFP-Schu S4 detected by flow cytometry was primarily intracellular since the addition of trypan blue prior to analysis did not significantly change the percentage of infected cells (data not shown).
Schu S4 elicits moderate phenotypic maturation of human DCs.One DC function is antigen presentation to T cells. This function is concomitant with increased expression of several surface receptors including HLA-DR, HLA-ABC, CD86 and CD83, a process also known as phenotypic maturation (42). One evasion strategy employed by successful pathogens is to interrupt this phenotypic maturation. Thus, we evaluated changes in DC surface expression of several DC receptors following infection with Schu S4. Forty-eight hours after infection, Schu S4-infected DC cultures had significantly more (P < 0.01) HLA-DR, HLA-ABC, CD83, and CD86 on their cell surfaces than untreated controls (Fig. 2). However, this increase was significantly less than that observed with cells stimulated with E. coli LPS (Fig. 2). This increase in receptor expression reflects changes in the entire cell population (uninfected and infected cells). However, similarly increased expression of HLA-DR, CD83, and CD86 was observed among Schu S4-infected cells, while HLA-ABC expression was decreased in approximately 20% of these infected cells (data not shown).
Schu S4 does not induce production of pro- or anti-inflammatory cytokines from DCs.In addition to phenotypic maturation, another primary function of DCs is secretion of cytokines to aid in alerting or regulating the immune response to invading pathogens. DCs recognize microbial products via an array of pathogen recognition receptors and secrete either pro- or anti-inflammatory cytokines following ligation of these receptors. Thus, we next determined if human DCs could respond to infection with Schu S4 via secretion of various cytokines previously shown to be crucial in developing effective immune responses against F. tularensis infections (13, 19).
Despite exponential replication and phenotypic maturation, we did not detect TNF-α, IL-12/IL-23p40, IL-6, or IL-1β at any time point (24, 48, or 72 h) after infection (Fig. 3 and data not shown). We along with others have observed induction of anti-inflammatory cytokines and type I IFN by F. tularensis following infection of antigen-presenting cells (7, 8, 26, 51). As expected, DCs responded to E. coli LPS by secreting IL-12, TNF-α, IL-1β, and TGF-β into culture supernatant (Fig. 3). However, we also failed to detect IL-10, TGF-β, prostaglandin E2, IFN-α, and IFN-β at any time point after infection of human DCs with Schu S4 (Fig. 3 and data not shown).
Schu S4 suppresses the ability of human DCs to respond to secondary stimulus.Given the striking lack of cytokine secretion in Schu S4-infected DCs, we next determined if Schu S4 was simply evading detection by human DCs or if it actively suppressed the ability of human DCs to respond to pathogen stimuli. At various time points after infection, we stimulated DCs with ultrapure E. coli LPS. DCs infected with Schu S4 failed to produce TNF-α or IL-12/IL-23p40/70 in response to E. coli LPS (Fig. 4A and B). A similar pattern of poor responsiveness was observed when infected cultures were exposed to zymosan and Pam3CSK4, suggesting that the inhibition among infected DCs was not limited to responsiveness to E. coli LPS but, rather, may be a more general phenomenon applicable to multiple pattern recognition pathways (Fig. 4B and data not shown).
To determine if live Schu S4 cells were required for the observed inhibition of responsiveness to E. coli LPS, we next examined the ability of paraformaldehyde-killed Schu S4 to induce or suppress production of cytokines by human DCs. Although dead Schu S4 did not elicit production of TNF-α or IL-12/IL-23p40/70, cells treated with killed Schu S4 were able to respond to LPS, as indicated by their ability to produce these cytokines in response to E. coli LPS (Fig. 5). This suggested that either metabolically active Schu S4, a molecule sensitive to paraformaldehyde degradation, or a molecule removed from bacterial preparations following washing of Schu S4 after fixation was responsible for suppression of DCs. Furthermore, the observation that killed Schu S4 was unable to elicit production of TNF-α and IL-12 from human DCs suggests that perhaps dying Schu S4 in vivo also fail to stimulate an inflammatory response.
Schu S4 infection does not preferentially induce apoptosis of human DCs in vitro.One explanation for the lack of proinflammatory cytokines and poor responsiveness to secondary stimuli is that the cells are undergoing apoptosis. Since activated DCs can display phosphatidyl serine (which binds annexin) on their surfaces, we opted to assess apoptosis by monitoring cells for cleaved caspase-3. Cleaved caspase-3 is a highly specific and early indicator of apoptosis. We did not observe increased cleaved caspase-3 staining in Schu S4-infected DC cultures compared to uninfected controls (Fig. 6A to E). In fact, among Schu S4-infected cultures, the majority of DCs positive for cleaved caspase-3 were negative for Schu S4 (Fig. 6C and D). Furthermore, there were significantly more cleaved caspase-3-positive cells in uninfected controls than in Schu S4-infected DC cultures (Fig. 6E). Thus, these data suggest that apoptosis of DCs is not the mechanism by which these cells fail to secrete proinflammatory cytokines and respond to microbial stimuli following Schu S4 infection.
Uninfected bystander cells in Schu S4-infected DC cultures respond poorly to microbial stimuli.Following infection with live Schu S4, we made the surprising observation that production of TNF-α and IL-12 among cells negative for F. tularensis in infected cultures was significantly less than that observed in uninfected cultures stimulated with E. coli LPS (Fig. 4A and B). The percentage of Schu S4-negative cells that failed to respond to E. coli LPS could not be accounted for in the GFP-Schu S4-positive population. It is possible that the GFP-Schu S4-negative cells harbor 1 to 2 bacteria and therefore appeared uninfected. However, the idea that the presence of such a small number of bacteria per cell exerted a significant effect on the ability of DCs to respond seemed unlikely. Thus, we reasoned that live Schu S4 may be mediating suppression of bystander DCs indirectly. Following infection and replication in DCs, Francisella infects new cells by lysing the primary cell and infecting the next nearest cell. Thus, Francisella spends at least a portion of its life cycle in the extracellular milieu. Viability of the bacterium as it spreads from cell to cell in the extracellular compartment is essential for successful reinfection of bystander cells since retention of high doses (10 to 50 μg/ml) of gentamicin in cell culture over time effectively inhibits infection of bystander cells. Francisella is also capable of limited replication in tissue culture medium. Thus, the suppression we observed in Schu S4-negative bystander cells may have been a result of the replication of bacteria in the extracellular space prior to reinfection of bystander cells. To determine the contribution of extracellular replication of Schu S4 on suppression of responsiveness to TLR agonist, we infected DCs as described in the Materials and Methods and added gentamicin at the reported MIC (4 μg/ml) approximately 15 h prior to analysis of responsiveness to E. coli LPS. Addition of gentamicin at this time point significantly reduced the number of viable bacteria in the medium of infected DC cultures (Fig. 5A). As expected, reduction of viable bacteria in the extracellular compartment resulted in fewer infected DCs (Fig. 7A). As previously shown, Schu S4 significantly inhibited production of both TNF-α and IL-12 in directly infected and uninfected bystander cells (P < 0.01) (Fig. 7B). Presence of gentamicin did not reverse the suppression of TNF-α and IL-12 production among directly infected DCs (Fig. 7B). However, limiting extracellular replication of Schu S4 with gentamicin restored the ability of uninfected bystander cells to produce TNF-α in response to E. coli LPS (Fig. 7B). Interestingly, limiting extracellular replication of Schu S4 did not restore the ability of human DCs to produce IL-12 in response to E. coli LPS. Together, these data suggest that extracellular bacteria may play an active role in inhibiting TNF-α responses but that the suppression of IL-12 is not as tightly controlled by viable bacteria in the extracellular space.
Suppression of DC responsiveness following infection with Schu S4 is not due to IL-10 or TGF-β.IL-10 and TGF-β are two host cytokines previously associated with suppression of induction of proinflammatory responses (32, 39). Although we did not detect these cytokines in our Schu S4-infected DC cultures, it is possible that they were present in concentrations that were physiologically active but below the level of detection. Thus, to determine if IL-10 and TGF-β were contributing to poor DC responsiveness following infection with Schu S4, we added neutralizing anti-IL-10, anti-pan TGF-β antibodies, or the appropriate isotype control to Schu S4-infected DCs and assessed responsiveness to E. coli LPS. Neither addition of neutralizing anti-IL-10 nor anti-TGF-β antibodies restored the ability of Schu S4-infected human DCs to respond to E. coli LPS, as measured by production of TNF-α and IL-12 (Fig. 7). Thus, neither of these host components was responsible for the inability of DCs to respond to secondary stimuli.
S4CM inhibits DC responsiveness.The inability of DCs in the presence of live Schu S4 to respond to secondary stimuli may stem from molecules that originate from the host, the bacterium, or both of these elements. However, we failed to detect several of the host-derived cytokines, e.g., TGF-β, IL-10 and prostaglandin E2, that are typically associated with eliciting anti-inflammatory or suppressive responses following infection with Schu S4. Furthermore, addition of neutralizing antibody against TGF-β and IL-10 did not restore DC ability to respond to secondary stimuli (Fig. 7). Thus, we reasoned that Schu S4-derived products may inhibit DC responsiveness to E. coli LPS. Unlike attenuated F. tularensis LVS, Schu S4 replicates logarithmically over 48 h in cRPMI medium in the absence of host cells (C. M. Bosio and D. Crane, unpublished observations). We took advantage of this trait to assess the ability of Schu S4 components that might be shed or secreted during extracellular replication to interfere with DC function. Following overnight incubation of Schu S4 in cRPMI medium, the resulting S4CM was sterile filtered and in some cases heated for 1 h at 95°C [S4CM(95)] and then tested for its activity on human DCs. Although no IL-6 was detected in the supernatants, unlike intact bacterium, S4CM elicited very low concentrations of both TNF-α and IL-12/IL-23p40 (Fig. 8A) into the culture medium. This stimulatory activity from S4CM was partially heat stable since cells incubated with S4CM(95C) secreted TNF-α and IL-12/IL-23p40 but at significantly lower concentrations than DCs incubated in S4CM (Fig. 8A). However, despite this weak cytokine response, S4CM had a strong inhibitory effect on DC responsiveness to E. coli LPS. Approximately one-third fewer DCs preincubated with S4CM were able to produce TNF-α or IL-12 in response to E. coli LPS compared to untreated controls (Fig. 8B and C). Unlike the induction of primary cytokine secretion, the inhibitory effect of S4CM on DCs was not completely lost following heat treatment (Fig. 8B and C), suggesting that the Schu S4 components responsible for suppressing responses to E. coli LPS in DCs were primarily heat stable.
Schu S4 LPS is weakly inflammatory and poorly tolerogenic for human DCs. F. tularensis is a gram-negative bacterium and, thus, possesses LPS. Given the heat-stable nature of the suppressive factor in S4CM, we next determined if purified Schu S4 LPS may be inducing endotoxin tolerance and, thus, mediating nonresponsiveness to E. coli LPS in human DCs. DCs were incubated with purified Schu S4 LPS followed by exposure to E. coli LPS. Schu S4 LPS did not elicit production of intracellular IL-12 or TNF-α at any concentration tested (Fig. 9A). Analysis of culture supernatants incubated with Schu S4 LPS overnight also failed to yield concentrations of TNF-α, IL-12, IL-6, or IL-10 above that observed in untreated controls (data not shown). Furthermore, only DCs exposed to high concentrations of Schu S4 LPS (10 μg/ml) were impaired in their ability to respond to E. coli LPS (Fig. 9B).
F. tularensis LPS does not contribute to inhibition of DCs by S4CM.LPS was detected in S4CM (Fig. 10A). Although our data show that concentrations of purified Schu S4 LPS 1,000-fold higher than the concentration of E. coli LPS are required to induce tolerance, it was possible that F. tularensis LPS was, in part, mediating the tolerance we observed in S4CM. Thus, we next depleted S4CM of Schu S4 LPS. As described above, S4CM inhibited the ability of DCs to produce TNF-α and IL-12 in response to E. coli LPS (Fig. 10B). Similarly, depletion of Schu S4 LPS in S4CM failed to restore DC production of these two cytokines following exposure to E. coli LPS (Fig. 10B). Furthermore, we quantified the Schu S4 LPS present in S4CM and found that it was present at less than 1.5 μg/ml. This concentration is nearly 10-fold less than what was required to induce refractory responses in human DCs (Fig. 9B). Therefore, it is unlikely that Schu S4 LPS alone present in S4CM was responsible for mediating nonresponsiveness of uninfected cells to unrelated LPS molecules. These data suggest that other heat-stable moieties may contribute to the poor responsiveness of Schu S4-negative cells observed in Schu S4-infected DC cultures.
DCs are a central component of the mammalian immune system and serve as both responders during innate immunity and a bridge to effective and long-lasting memory immune responses. Thus, it is unsurprising that many pathogens have developed mechanisms to modulate and disable DCs (1, 6, 33, 40, 45-48). One way in which pathogens interfere with host immune responses, including those mediated by DCs, is manipulation of normal host systems meant to limit hyperresponsiveness to microbial products, resulting in control of inflammation. For example, the temporary state of refractoriness to endotoxin and other microbial products following sepsis (referred to as "microbial tolerance") tempers the inflammatory response and development of septic shock (as reviewed in reference 35). However, this state of tolerance also leaves the host susceptible in a hyporesponsive state and, thus, more susceptible to secondary infection (23, 25, 34, 49). It has been postulated that some pathogens may use induction of tolerance as a mechanism by which to evade the immune response to successfully infect and replicate in the host (28). The specific mechanism(s) of microbial tolerance is varied and ill defined and has been suggested to operate at multiple levels from alteration of receptor expression to impairment of cell signaling pathways.
Data presented herein suggest that virulent F. tularensis may utilize microbial tolerance as a mechanism to evade elicitation of proinflammatory cytokines in human DCs, ultimately dysregulating the immune response in favor of the bacterium. Using GFP-Schu S4, we also observed that cells negative for this bacteria responded poorly to secondary stimulation with E. coli LPS. In contrast to previous reports with more attenuated strains of F. tularensis, we demonstrate that direct infection of DCs was not required to successfully interfere with DC responsiveness to multiple TLR agonists. It is possible that these cells harbored small numbers of GFP-Schu S4 cells that were below the threshold of detection. However, due to the magnitude of nonresponsiveness in Schu S4-negative cells and the ability of sterile, S4CM to inhibit DC responsiveness, we do not believe that small (1 to 2 CFU) numbers of undetectable GFP-Schu S4 cells were the primary contributors to tolerance in Schu S4-negative cells. Rather, our data suggest that in addition to modulation of infected cells, Schu S4 secreted or shed molecules that induced a refractory state in uninfected bystander human DCs. The specific mechanism of immunosuppression may be different among bystander and directly infected cells. However, both result in poor DC responsiveness and may contribute to the overall pathogenesis of Schu S4-mediated disease. Our observations of DC suppression represent an important advance in understanding how pathogens might manipulate these critical host cells. As described, the induction of microbial tolerance in human cells following exposure to microbial products is a well-established phenomenon. However, in the case of traditional tolerance, the pathogen stimulates an initial wave of proinflammatory cytokines which may serve to alert the host to the invading pathogen. Our data with Schu S4 suggest that highly virulent pathogens may have developed mechanisms by which they can effectively suppress cell responsiveness in the complete absence of proinflammatory cytokine production, thus evading both the initial wave of host effector responses as well as tempering the ability of the host to mobilize additional defenses. Furthermore, little is understood about how human DCs are modulated by virulent pathogens. Thus, data presented herein provide an important concept concerning modulation of primary DCs by highly virulent pathogens and should be considered when analyzing the interaction of these cells with other infectious agents.
The suppression of bystander human DCs presented here correlates with our previous findings in the murine model of pneumonic tularemia. In those studies, inhalation of Schu S4 inhibited the recruitment of proinflammatory cells throughout the lung in response to LPS (7). Importantly, this occurred at a point when infection was restricted to the airways, suggesting that fulminant infection of the lung was not required to exert organ-wide tolerance to LPS. Although we did not define the mechanism of unresponsiveness in that study, it is possible that direct modulation and induction of tolerance by Francisella products contributes to the unresponsiveness. Indeed, it has been observed that humans experimentally infected with virulent F. tularensis develop in vivo tolerance to LPS from other gram-negative bacteria (24). The specific mechanism of tolerance in humans infected with Francisella was not defined at the time of that study. However, with the recognition of TLRs as key receptors for recognition of LPS and other pathogen-associated molecular products, it is possible that Francisella is directly modifying TLR-mediated activity. Inhibition of TLR signaling and the resulting cytokine production may occur at several levels including decreased expression of TLRs on the cell surface, inhibition of phosphorylation of specific signaling molecules required for induction of cytokine production, and induction of TLR-negative regulators such as Tollip, suppressor of cytokine signaling 1 (SOCS1) to SOCS3 and IRAK-M (as reviewed in reference 29). The direct effect of Francisella on each of these steps in TLR signaling is currently being examined in our laboratory. Thus, although the murine lung environment is quite different from that of in vitro cultured human DCs, it is tempting to speculate that identification of the specific mechanisms involved in the inhibition of human DCs may also be at work in the murine lung. Thus, the data presented herein may provide important new clues as to how virulent Francisella, and potentially other important human pulmonary pathogens, might be influencing both directly infected cells and uninfected bystanders.
Although a number of microbial products are capable of inducing modulating immune responses, the most well-studied molecule is LPS (as reviewed in references16 and 20). F. tularensis is a gram-negative pathogen and, thus, possesses LPS. While high concentrations of purified Schu S4 LPS could suppress human DC responsiveness, further depletion of LPS from S4CM failed to restore responsiveness of human DCs to unrelated TLR agonists (E. coli LPS) (Fig. 6 and 7). The poor stimulatory capacity of Schu S4 LPS is in agreement with previous reports examining immunogenicity and the tolerogenic capacity of LPS derived from the more attenuated F. tularensis strain LVS (2, 17). However, it is well established that optimal induction of signaling via E. coli LPS in mammalian cells requires both CD14 and LPS binding protein (LBP). Although E. coli LPS is capable of stimulating primary human DCs in the absence of these two proteins (Fig. 3 to 5, 8, 9, and 11), it is possible that CD14 and LBP are required for cellular activation or suppression mediated by Schu S4 LPS. Both CD14 (cell membrane bound and soluble) and LBP are present in abundance in vivo. Thus, while Francisella LPS does not play a predominant role in the induction of tolerance in host macrophages and DCs in vitro, it may exert a more profound effect in the in vivo setting. Furthermore, there may be other heat-stable Schu S4 components capable of mediating tolerance to multiple microbial TLR agonists in vitro and in vivo that were not identified in this study. Identification of these components is currently being pursued in our laboratory. This identification will enable us to develop novel therapeutics and vaccines against tularemia. Additionally, given the strong suppressive activity mediated by these molecules, they may also represent a useful class of anti-inflammatory agents capable of dampening destructive inflammatory responses present during other diseases.
In addition to microbial tolerance, there are other potential bacterial components and mechanisms that may contribute to the suppression of human DC activity. F. tularensis encodes a pathogenicity island (FPI) that is critical for survival and replication of the bacterium (36, 37, 43). Specifically, several of these genes have been shown to be important for F. tularensis escape from the phagosome, enabling replication of the bacterium in host cell cytoplasm (43). Interestingly, one gene and the resulting protein have been implicated in both phagosomal escape (resulting in replication of the bacterium) and induction of tolerance in murine and human macrophages. LVS bacteria lacking the iglC gene failed to inhibit responsiveness to E. coli LPS following infection of J774.1 macrophages (50). Furthermore, a spontaneous LVS mutant that failed to produce IglC induced both proinflammatory cytokines and was unable to suppress responsiveness of human macrophages to E. coli LPS (11). We detected IglC protein in S4CM. However, depletion of iglC from S4CM failed to restore responsiveness of human DCs to other TLR agonists (data not shown). This suggests that IglC alone is not responsible modulation of human DC.
The FPI also encodes a type VI secretion system. In other bacteria, type VI secretion systems are responsible for secretion of molecules that are capable of disabling the host immune response. For example, proteins secreted via the type VI secretion system described in Vibrio cholera are responsible for cytotoxicity in mammalian macrophages (38). Porphyromonas gingivalis utilizes type VI secretion to expel gingipain proteases. Interestingly, an important function of these proteases is the induction of LPS tolerance in macrophages (18, 41). Type VI secretion systems have also been identified in Yersinia and Burkholderia species (44, 52). While their presence is associated with virulence, the specific effectors and their mechanisms of action on a cellular level have not been defined. A similar phenomenon may be at work in Francisella. That is, in Francisella species, it is possible that while IglC may have a role in phagosomal escape, it is not the effector molecule mediating hyporesponsiveness. Rather, IglC may act as part of a type VI secretion apparatus that aides in the delivery of a yet to be defined effector molecule ultimately responsible for inhibiting host cell responsiveness to inflammatory stimuli. Additional studies examining the specific role of IglC and other proteins encoded in the FPI in the induction of Francisella-mediated tolerance are currently under way in our laboratory.
As a facultative intracellular pathogen, F. tularensis must contend with the host immune system from both inside and outside individual host cells. It is likely that the mechanisms by which F. tularensis accomplishes this are complex and involve a number of strategies. Here, we show for the first time that one way in which virulent F. tularensis interferes with host immunity is by suppressing responsiveness of both directly infected cells and uninfected bystander cells. Interestingly, in contrast to the production of an array of proinflammatory cytokines observed in cells exposed to other microbially derived TLR agonists such as LPS or peptidoglycan prior to the onset of unresponsiveness, the Schu S4 LPS and other components present in the culture medium were only weakly inflammatory. Thus, the profound suppression mediated by F. tularensis in DCs was not obtained at the cost of an initial burst of cytokines that might alert the immune system. Importantly, the broad suppression of DC responsiveness (in terms of cytokine secretion) is similar to that observed in the lungs of mice following aerosol infection with Schu S4 (7). Together, these data suggested that Schu S4 suppresses the host immune response in a global sense; that is, interference with host responsiveness is not restricted to infected cells but extends to uninfected cells that may aid in the resolution of infection. These data also have broad implications for how both human DCs and the murine pulmonary environment are manipulated by virulent pathogens and represent an important consensus of global dysregulation by a pathogen in murine and human cells.
We thank Paul Brett for guidance and assistance in preparation of the Schu S4 LPS. We also thank John Belisle and Brian Kelsall for their helpful discussion and criticism pertaining to this work. Also, we thank Steven Holland, Eugene Howerton, and the Department of Transfusion Medicine at NIH for their assistance in providing human monocytes.
This work was supported by the Intramural Research Program of the National Institutes of Health, National Institute of Allergy and Infectious Diseases.
- Received 16 July 2008.
- Returned for modification 1 September 2008.
- Accepted 26 October 2008.
- Copyright © 2009 American Society for Microbiology


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It was an exciting afternoon in our classroom. Several weeks ago I received an out of the blue email from Jessie DeVito asking is she and her husband, New York Jets defensive end Mike DeVito, could visit our classroom as a special surprise for their niece. When they arrived today, I saw the biggest smile that I have ever seen on my little kindie's face.
What a nice couple. Mike seemed very humble and kind. Jessie, also very sweet, actually grew up in our town and went to our school when she was little. They both came in with smiles on their faces and patient demeanors, comfortable with all of the energy in our room. Mike sat in my old wooden rocker and read The Runaway Bunny, one of his favorite books when he was in kindergarten, to a class full of very excited kindies. Jessie, led by the hand by her little niece, sat criss cross applesauce on the rug, and her niece snuggled close to hear the story.
Well, after story everyone had the chance to check out Mike's helmet and a real NFL football. That helmet looked so big in those little hands! When Mike asked if anyone had any questions (and you all know the way kindies question), one little guy said "I really like your sneakers, and they sure are big!" Mike just smiled and agreed that they certainly were.
Jessie had asked for a list of first names of the children in our class, because they wanted to bring each child an autographed photo. Well, I was stunned at the wonderful gifts they brought for all of the children, including their own copies of The Runaway Bunny. I think this was a visit the class will talk about all year long. And let me tell you, this kindergarten teacher is going to take advantage of the excitement. I am going to spend the weekend making some football related centers and planning all the writing activities I can think of related to our very special visitors.
Special thanks to Mike and Jessie DeVito for creating a wonderful experience for my kindies!
Mrs. B.


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Resist the urge to move the meat around before it's seared or it won't get that nice, brown crust—the ideal texture.
How to Make It
Warm a 12-inch skillet over medium-high heat. Season steaks with salt and pepper. Swirl 2 tsp. oil in skillet. Add steaks; cook until browned on one side, 3 to 4 minutes. Turn and cook, 3 to 4 minutes longer for medium-rare. Transfer to a platter and tent with foil to keep warm.
Add remaining 2 tsp. oil, white and light green scallion pieces and ginger to skillet; sauté for 1 minute. Add garlic; sauté for 30 seconds. Add sherry and broth; cook, stirring, until liquid has reduced by about half, 30 seconds to 1 minute. Stir in oyster sauce. Remove skillet from heat; add butter and swirl until sauce is creamy.
Slice steaks across grain; spoon sauce over. Top with scallion greens and sesame seeds and serve.


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Unscrambling Egg Labels
I've always believed that happy hens lay the healthiest eggs. However, the labels on the cartons can often be more confusing than helpful: should we be looking for cage-free, free-range, or is organic the way to go?
If the homeowners association where I live wasn't so strict, there would already be a couple of hens sunning themselves in my backyard. But until the rules change (or I can persuade someone living close by to take on raising chickens), I'm going to have to be more diligent about which eggs I choose at the store.
Despite some pretty hairy documentaries showing an alarming side of farming, there are still good people out there who care about their chickens. Here's a brief guide to what the labels really mean. It looks like certified humane, pasture raised, or organic are the best choices - and worth paying extra for.
Also, don't forget about your local farmers market: it's a great place to find good fresh eggs without having to plow through labels.
I just have to add that although egg yolks contain cholesterol, they also have an abundance of nutrients (including omega 3's, and hard to find vitamin D.) So, unless you've been advised by your doctor to avoid them, do you really want to throw away the most nutritious and delicious part of the egg? I think not. And with that in mind, I'm off to make myself a nice dippy egg!
* Please always follow your doctor's advice if you have a medical condition.
Consumer Reports "Pasture Raised"
Animal Welfare Approved
Certified Humane
Global Animal Partnership
Although I have no formal education in nutrition, I've been researching this subject for over forty years. Healthy eating is my passion, and I love to share what's worked so well for me.
February 2020


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Final Fantasy XIV's Make it Rain Campaign returns today which brings a 50% boost to all MGP rewards in the Manderville Gold Saucer. A new quest is available there that sheds some light on the roaming Senor Sabotender.
You can find the quest chain to start the event below.
Via The Lodestone:
- The Sabotender Shimmy
From: Thursday, June 6th, 2019 @ 1:00am Pacific Daylight Time
To: Monday, June 24th, 2019 @ 7:59am Pacific Daylight Time
Location: Lamenting Lalafell @ Ul'dah – The Steps of Nald (X:9.4, Y:9.2)
Character Requirements: Level 15
Quest Requirements: "The Gridanian Envoy," "The Ul'dahn Envoy," or "The Lominsan Envoy." (2.0)
Event Rewards
- Emotes:
Senor Sabotender
MGP Gold Card (30,000 MGP)


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Oct 29th 2015
They're having a baby!
Conceiving a child is an exciting time. Some couples wait until they are through the first trimester to announce, while others can't wait to get the word out as soon as the the test comes back positive. Are you ready to divulge your baby news?
Here are 20 of our favorite pregnancy announcements:
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Haven't posted for several days, busy taking-care-of things. Some thought-provoking moments, but having a hard time bringing things into focus; maybe I'm reading too many novels.
Spent a few days visiting my mom. She has "a" glioblastoma, diagnosed 3 1/2 years ago, and is struggling with the effects of long-term chemo, the latest "round" having gone on now for a year. She's looking forward to the doctor-recommended break and hoping that it will allow her to regain some energy, but is also afraid that it will give the tumors a chance to grow. It is, and has been, a mixed blessing, because she has far exceeded the usual prognosis for this type of cancer, but the chemo is really wearing her out. My daughter and I gardened for her (she's trying to sell her house, and her yard looks like something from a magazine, which is especially remarkable considering she can only work in 20-minute increments. She quoted my beloved great-grandmother to me: "I work for a while, then rest for two whiles.") The next day I scoured her rather large deck and harvested lilac sprouts to bring home and plant in my yard. Exhausting, but good, honest work, and allowed me to reconnect with muscles I had forgotten about.
Yesterday I watched world cup soccer with my husband, and ordered flooring for our upcoming house-remodel project (old laminate crap and filthily disgusting mold-and-dust-and-pet-hair ridden carpet being exchanged for travertine and bamboo). Then we planted the lilacs, hoping the rampaging deer will leave them alone, and edged the flower bed. Another day of good, honest work, (GHW), and have become acquainted with even more muscles.
Today we decided that we couldn't put all those beautiful floors in and not do something about the kids' computer desk — a desk I tried to refinish once by painting it white to match the cupboards, but hadn't managed to remove enough finish first so it basically peeled like a kid with a bad sunburn. Or glue — remember when you were a kid and painted glue on your hands so you could peel it off when it dried? My daughter had decided, helpful girl, that the desk looked better without the paint, so systematically peeled little tiny bits of it whenever she was at the computer, creating a wonderfully skin-diseased mottled effect. So my husband and I worked lengthily with hazardous, toxic chemicals, taking turns dashing into the house to wash the caustic substance off every time it dripped on us, and scraped and scoured and scrubbed. Still not sure it's going to "work" but at least the paint's off and we're looking at mostly bare wood. I've now become acquainted with even aNOTHER set of muscles and have minor chemical burns on my arm. Tomorrow we get to start sanding! Yippee!!
At the end of the day's exertions I made us a pitcher of strawberry margaritas (with half the tequila I used in the last batch; we're too old to get hammered before dinner) and, sitting on the deck and enjoying a beautiful June evening, finished reading The Other, by David Guterson. A lovely book: two young men, one privileged, one middle-class, become friends in high school. The privileged boy, John William, raised by a mentally-ill mother and an emotionally absent and ineffective father, becomes more and more eccentric through high school and the beginnings of a college education, until he becomes a complete recluse and lives in a limestone cave in the Pacific Northwest "bush." His friend and blood-brother Neil Countryman (a less-than-subtle but effective name which implies every-man, and the down-home values of the peasant) visits, and supplies, him on occasion while pursuing a middle-class life ("selling out to Hamburgerland"): high school English teacher, wife, two sons. John William dies, and is eventually found, at which point it is revealed that he has left $440 million to his friend. Neil and his wife struggle with what to do with this money, what will it change? What would they like to stay the same? Can it?
Eventually. . ."Jamie and I turned in the '92 Civic and bought a hybrid, which we recently took to the Canadian Okanagan. . .We walked, swam, biked, sunned, tasted wines, ate well, bought pottery, and watched the sun go down, and though all of this was fun, none of it made us happy. We both wanted something else that was unnamable. It might be forever unnamable. In this regard, money changes nothing, which Jamie and I knew before we had it."
Neil is an avid reader, and does find that the inheritance encourages his tendency to indulge at used-book stores. Near the end of the book he recounts some of the wisdom imparted to new parents by Dr. Benjamin Spock:
1. You know more than you think you do.
2. Parents are human — they have needs.
3. Some children are a lot more difficult than others.
4. At best, there's a lot of hard work and deprivation.
5. Needless self-sacrifice sours everybody.
6. Parents should expect something from their children.
7. Parents are bound to get cross.
to which I think
1. Maybe; but maybe I know less and then we're all screwed.
2. Definitely. Forgot it for about 20 years. . .
3. Ya' think?
4. Ditto.
5. Yes, it does.
6. And be willing to wait 25 years to get it.
7. Phew!
And so on, to the final line of the book, which is "It's not the words but the music that counts."
I like that.


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Congratulations to: DW, DA, DM and DN who are through to the grand final! Please make a note of the date: Wednesday March 7th 6.30-9pm in A block hall! Points will be awarded for the numbers of participants for each house so make sure you are there. There will be a rehearsal before the concert and letters will go out after half term. Well done to EVERYONE! An excellent competition this year
Mrs G


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Q House Sukhumvit79
Q House Sukhumvit79
Q. House Condo Sukhumvit 79 is a condominium project, developed by Quality Houses, located at 2045/6 Sukhumvit Rd, Khwaeng Phra Khanong Nuea, Khet Watthana, Krung Thep Maha Nakhon 10110. Quality Houses is also the developer behind The Trust Condo South Pattaya, Sathorn House and Casa Condo @ CMU. Construction of Q. House Condo Sukhumvit 79 was completed in 2014. Condominium comprises of a single building, having 27 floors and includes 484 units.
Q. House Condo Sukhumvit 79 conveniently located just within 250 m or about 4 minutes walk from the On Nut. If you drive, the nearest tollway entrance is located 1.5 km from the condo.
Numerous shops are situated within reach:
- Market Plus Shopping Center is 580 m away (approximately 7 minutes by foot)
- Phra Khanong Plaza Show Room – 1.1 km (11 minutes by car)
- Jusco Department Store (Sukhumvit 71) – 1.8 km (12 minutes by car)
- MaxValu – 2.3 km (10 minutes by car)
- Maxvalu Department Store (Ekkamai) – 2.7 km (13 minutes by car)
Also a Family Mart convenience store, located just 2 minutes walk away, will satisfy residents's needs for everyday items shopping.
The closest schools in proximity to Q. House Condo Sukhumvit 79 include:
- Saint Michael's International Kindergarten, located within 400 m away (approximately 5 minutes by foot)
- Sanghirun School – 420 m (6 minutes by foot)
- Wells International School Onnut Branch – 680 m (8 minutes by foot)
- Athiphon Kindergarten – 800 m (9 minutes by car)
- Panaya Kindergarten – 1 km (4 minutes by car)
Room for rent at Q house 79 [Just100m. from BTS Onnut]
Type : 1 Bedroom [30 sq.m.]
High floor, City view
Fully furnished
High quality furniture
LED TV, Refrigerator , Microwave, Washing Machine included
Location and Transportation :
100m. BTS Onnut Station
150m. Tesco Lotus Sukhumvit 50
150m. Century the movie plaza Sukhumvit
Just 3 stations to BTS Ekkamai
Just 4 stations to BTS Thonglor
Rental : 21,000 THB/month
Minimum 1 year contract [2 months Deposit + 1 month Rental Advance]


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- Description
MXR Cables are designed with musicians in mind, both rugged and tonally accurate they allow the transfer of the purest signal from the guitar to destination whether that be to an amp or pedal board or studio.
OFC for pure tone
Oxygen-free copper cabling and shielding keep your signal purity at its highest while minimizing cable interference from other electromagnetic sources. The PVC jacket helps with noise rejection while maintaining the rugged reliability of MXR Cables.
- Specification
Manufacturer MXR by Jim Dunlop Model JD-DCIS20 Colour Matte Black Length 20ft
- Reviews
Write Your Own Review


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ecoEd integrate digital tools for Environmental Sciences in Tertiary Education. ecoEd is a partnership between the Atlas of Living Australia (ALA), the Terrestrial Ecosystem Research Network (TERN), the Biodiversity and Climate Change Virtual Laboratory (BCCVL), ecocloud, the online platform for the ecoscience community, the Australian Bureau of Agricultural and Resource Economics and Sciences (ABARES) and the Australian Research Data Commons (ARDC). Each of these partners provide training material that is accessible online through the ecoEd website, and participate in delivering training to ecoEd Champions.
The Award Winners will be announced on Wednesday 22 May