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Helga Obremski, 77, Stevens Point, died Friday, Aug. 29, 2014, at Aspirus Hospital in Wausau.
A Mass of Christian Burial will be held at 10:30 a.m. Thursday, Sept. 4, at St. Casimir Catholic Church in the town of Hull, with the Rev. Arul Joseph V. officiating. Burial will be in the parish cemetery.
Visitation will be at the Pisarski/Dzikoski Funeral Home in Stevens Point from 4 to 8 p.m. Wednesday, Sept. 3, and at the church from 9:30 a.m. Thursday until the Mass. A rosary will be prayed at 7 p.m. Wednesday at the funeral home.
Memorials in her name will be established at a later date.
Condolences may be offered online at www.pisarskifuneralhome.com.
Mrs. Obremski was born Oct. 1, 1936, in Kaiserslautern, Germany.
She was married to John Obremski Jr. Oct. 11, 1963, in Germany.
They settled in Stevens Point.
She worked at the University Center on the University of Wisconsin-Stevens Point campus as a cook.
Survivors include her husband, John; three children, John (Nicole) Obremski III, Brenda (Duane) Cartwright, Troy (special friend, Jessica Gilmeister) Obremski; one sister Trudy (Andy) Reed; one son-in-law, Anthony (Kathy) Poole; three grandchildren; and one great-grandson.
She was preceded in death by one daughter, Patricia Poole; two brothers, Munfred Kraus and George Kraus; and one sister, Maria Wild-Englehardt.


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The DS420, popularly known as the Daimler Limousine, was the last of the large formal limousines produced by The Daimler Company Limited between 1968... More
Daimler SP250 1961 A Serie. Full frame-off restored in the 2000. Features including 4-Speed manual transmissions and a hardtop. This car won lot of... More
1961 Daimler SP250 '61 Daimler SP250, old English white with black interior, straight body, lots of potential, and an excellent original blue plate California car. For... More
One of Daimlers wonderful luxury platforms during the first half of the 1950s was known as the Regency. The standard Barker saloon body resembled... More

subset: commoncrawl


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27 of the Weirdest, Trendiest, Most Appetizing Popcorn Flavors Around
Exotic new flavors are a trend in all types of snack foods, and popcorn — that classic American movie theater treat — is no exception. Up your enjoyment of this fun, fluffy food by trying one of these tasty gourmet variations or daring flavor combinations.
Looking for a healthy way to satisfy your craving for something savory? Give one of these low-calorie snacks a try.
By Lauren Haslett
Spiced Almond Caramel Popcorn
In addition to this sweet and slightly spicy version, California-based company CC Made also makes a classic caramel corn and a pistachio-studded variety, as well as caramels and caramel sauces. The Spiced Almond, though, is a big seller, and balances the sweetness of the caramel with hits of cayenne and paprika. CC Made sells larger packages as well as 3-ounce sizes (pictured) that are ideal for snacking without going overboard.
Courtesy of CC Made


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The following are the statistical highlights of the third match of the tri-nation series between India and Bangladesh, played at the Sher-e-Bangla Stadium. #India's match-winning total of 297 for four is their second highest against Bangladesh - the highest being the 348 for five at Dhaka on December 27, 2004. # Bangladesh (296 for six) have posted their highest total against India. # Bangladesh's aforesaid total is also their highest at the Sher-e-Bangla National Stadium, Mirpur. # Tamim Iqbal (60 off 42 balls) has registered his highest innings against India. # Mahmudullah and Naeem Islam added 58 (unbroken) for the seventh wicket -- Bangladesh's highest against India. # Virat Kohli (91 off 102 balls) has posted his fourth fifty -- his first against Bangladesh. # Kohli's magnificent 91 is his highest innings on foreign soil. # Kohli's aforesaid innings is the second best by an Indian on debut against Bangladesh, next only to Yuvraj Singh's unbeaten 102 in Dhaka on April 11, 2003. # Mahmudullah's unbeaten 60 is his career-best innings in ODIs. # India's six-wicket triumph is their 11th out of 12 contested against Bangladesh in Bangladesh. # Mahendra Singh Dhoni's first hundred against Bangladesh is his seventh in ODIs, his fourth as captain and his sixth in a winning cause. # Dhoni is the only ODI captain to have averaged over 60 and over 80 in a winning cause as a batsman. # Imrul Kayes (70 off 100 balls) has posted his first fifty in ODIs. # Tamim has recorded his fifty in only 33 balls -- the fastest for Bangladesh against India in ODIs. # Tamim and Imrul Kayes have set a record with their 80-run stand for the first wicket against India. # Kohli and Dhoni put on 152 -- India's highest for the fourth wicket against Bangladesh. # Suresh Raina and Dhoni put on 94 -- India's highest for the fifth wicket against Bangladesh.
India, Sri Lanka, B'desh: Tri-series (Full Coverage)
Statistical Highlights of Ban vs Ind, Match 3
|Mirpur, 2010/Jan/08 06:00:00
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Ind v B'desh, 1st Test: Day 4 StatisticsStatistical highlights on fourth day of the first Test between India and Bangladesh.
Dhoni remains at the top; Raina, Kohli move upDhoni maintained his top position in the ODI batsmen rankings, while Raina and Kohli made big strides thanks to their recent good shows.
Indian cricketers to give monetary help to hockey teamThe Indian cricketers were discussing the idea of giving Rs 1 crore to the national hockey team who is facing a severe plight.
Statistical Highlights of Ind vs SL, FinalRaina's century in a losing cause, Sangakkara's best series as captain and more in the statistical highlights.
One series win does not make us great: SangakkaraKumar Sangakkara was happy with his side's performance but said they need to work harder in the year ahead.
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The California State University requires all students to take the English Placement Test and the Entry Level Mathematics test prior to enrollment in the California State Universities unless they are exempt by means of scores earned on other appropriate tests such as the ACT, AP, EAP and/or SAT. Although your EPT and ELM test scores are not requested as part of your admissions application to the university, you must satisfy the requirement before enrolling in classes.
Unless exempt, you must take the EPT and ELM tests by May 2, 2015 for fall 2015 enrollment. Because of heavy demand and limited seating, you should sign up for the tests much earlier than the May deadline. If you are required to take the EPT and/or the ELM but fail to do so, you will not be allowed to enroll at California State University, Northridge. If you do not perform well on the test(s), you will be placed in an appropriate developmental program during your first term of enrollment.
General Information
The English Placement Test is designed to assess the level of reading and writing skills of students entering the California State University. The California State University EPT must be completed by all non-exempt entering undergraduates prior to enrollment in any course including remedial courses. At CSUN, students who score 147 or above on the EPT will be placed in a one-semester college-level writing class. Students who score 146 and below will be placed in a two-semester college-level writing class.
The EPT requires approximately 1 hour and 45 minutes to administer and contains the following three sections.
- Essay: 45 minutes on an assigned topic
- Reading skills: 30 minutes to answer 45 multiple-choice questions
- Composing skills: 30 minutes to answer 45 multiple-choice questions
The first section asks you to write an essay. The next two sections assess your ability to comprehend and interpret reading material and your understanding of sentence construction and paragraph development.
To be exempt from the EPT, students must present proof of one of the following:
- A score of "Exempt" or "Ready for college-level English courses" on the California State University Early Assessment Program taken along with the English Language Arts California Standard Test in grade 11
- A score of "Conditionally ready for college-level English courses" or "Conditional" on the California State University EAP taken along with the English Language Arts California Standard Test in grade 11, provided successful completion of the Expository Reading and Writing Course, AP English, IB English or an English course approved for extra honors weight on the University of California "a-g" Doorways course list
- A score of 500 or above on the critical reading section of the College Board SAT Reasoning Test
- A score of 22 or above on the American College Testing English exam
- A score of 3 or above on either the Language and Composition or Composition and Literature examination of the College Board Scholastic Advanced Placement Program
- Completion and transfer to California State University of the credits for a college course that satisfies the California State University general education requirement in English composition, provided such a course was completed with a grade of "C" or better
Note: The College Board SAT I and SAT II were renamed SAT Reasoning and SAT Subject Tests, respectively, beginning March 2005.
Students who qualify for an exemption that is not reflected in university records should check to see if the qualifying score was sent to CSUN when the test was taken. Contact ETS at (925) 808-2142 to double check where your scores were sent. If your scores have not been reported to CSUN, send a copy of your qualifying test scores to the address below so the exemption can be documented on your permanent academic record at CSUN. Please remember to keep a copy of the exemption notice for your records.
Admission and Records
California State University, Northridge
18111 Nordhoff St.
Northridge, CA 91330-8207
Test Dates
All 23 California State University campuses administer the EPT (and the ELM) on a variety of variable dates. For a complete listing, check the California State University EPT/ELM Information bulletin. Pay close attention to the registration deadline listed by each test date since your registration must reach the testing office by the registration deadline.
Students may take the test at the most convenient California State University campus. Online registration is available for all campuses.
If you wish to take the EPT at CSUN, online registration is available. It is highly recommended that you test by one of the test dates listed below.
CSUN EPT and ELM testing calendar
|Test Date
|Registration Begins at 8 a.m. on
|Registration Ends at noon on
|February 14, 2015*
|November 17, 2014
|January 30, 2015
|March 21, 2015*
|November 17, 2014
|March 6, 2015
|April 11, 2015
|January 25, 2015
|March 27, 2015
|May 2, 2015*+
|March 1, 2015
|April 17, 2015
|June 20, 2015
|March 29, 2015
|June 5, 2015
*System-wide EPT and ELM test dates.
+Last day to take EPT and ELM for fall 2015 enrollment.
For information on specific exam time and location, visit the Testing Calendar page.
The English Placement Test is given in conjunction with the Entry Level Mathematics exam. Online registration is available for all campuses. Go to the California State University EPT/ELM Information bulletin for a complete list of EPT and/or ELM test dates and registration procedures.
If you wish to take the EPT at CSUN, online registration is available.
There is an $18 charge for the EPT, payable when you register for the examination. Students who are unable to pay online via credit card, Paypal or e-check, must contact ETS at (925) 808-2142 for an alternate payment method. No student will be tested without proper payment and picture identification.
Testing Accommodations
Accommodations for Students with Disabilities
Alternative testing accommodations such as extended time, electronic text, readers or scribes are available through the Disability Resources and Educational Services (DRES) department to students that have a documented disability and require accommodations to take the exam. If you are not a registered student with DRES and have a disability, please visit the DRES website for registration procedures.
In order to receive testing accommodations for the EPT and/or ELM tests, you will need to contact Disability Resources and Educational Services to provide proof of a disability and to schedule the tests. After review of your documentation, DRES will contact you to make an intake appointment with a disability counselor. This appointment should be scheduled at least 14 days prior to the EPT and/or ELM tests. To ensure all accommodations are in place for your tests, it is imperative that you contact the DRES office as soon as possible. Please understand that without the disability documentation and intake appointment we are unable to provide the requested accommodation.
Accommodations for Religious Observances
Non-Saturday testing is available for religious observances. If your religious observance prevents you from taking the test on the scheduled test date, students must sign up for the EPT online and contact the Testing Center to receive alternate testing arrangements at (818) 677-2369. Be prepared to provide documentation. The university EPT registration deadlines apply to all students, and accommodation requests must be submitted by the registration deadline.
Test Day
- Students should report to the location listed on their admission ticket. Rooms are assigned on site.
- Plan to arrive at least 15 minutes prior to your test time to allow for parking.
- Current photo ID (driver's license, student ID, passport, etc.)
- Several #2 pencils
- Know your social security number (do not bring your card)
- Your printed admission ticket
Visit our Test Reporting Locations Map for driving directions to all on-campus testing locations.
Out of State Testing
Students who are non-California residents and are unable to test at one of the California State Universities and need to test in their home state, must register online at the ETS website and select the test campus as "Out of State." Please note that there is an out of state testing fee of $75 in addition to the testing fees.
Test Scores
After you have taken the appropriate placement tests, schedule an appointment with your advisor to select the appropriate course(s) to enroll in for your first semester at CSUN.
Total test score: Your total test score is the combined scores of all three sections. It will indicate whether you have the skills in reading and writing that will permit you to perform according to the standards expected of you in regular college writing courses. A low total score indicates that you should enroll in a class and/or laboratory designed to improve your skills.
Reading skills score: Your score on the reading skills section of the test will indicate whether you are reading on a college-entry level or whether you should receive special instruction in reading.
Composing skills score: Your score on the composing skills section of the test will indicate your ability to select sentences that establish clear meaning, your knowledge of sentence structure according to the conventions of standard written English at the college-entry level, and your ability to recognize statements that support or help develop a given idea.
Essay score: Your score on the essay will indicate whether you have the skills necessary to write in-class papers or examinations in college.
Because the EPT is a placement test, scores determine what courses students must attend. The chart below will help you and your advisor select the appropriate course:
|EPT Score
|Course Placement
|139 and below
|ENGL 113A/UNIV 061 followed by ENGL 113B/UNIV 062
|ENGL 114A followed by ENGL 114B
|147 or higher
Failure to complete the required developmental courses in two semesters will result in disenrollment from CSUN. For information about compliance policy, consult the California State University Executive Order 665.
Helpful Sample Materials
To find out more about what's on the test, see Focus on English, which provides information about the entry-level English requirement of the California State University EPT test. The document explains scores on other tests that will exempt students from EPT and it includes answers to a number of frequently asked questions. The Focus on English pamphlet includes samples of the types of questions appearing on the new EPT test, as well as examples of essays and how they were scored. (Note: You will need Acrobat Reader to view these documents. It is available as a free download.)
See the California State University English Success website for test review questions.
Additional Information
Additional details may be found at the official California State University EPT/ELM website or the Online ETS Bulletin.
We have also provided a list of EPT and ELM FAQs for any additional questions you may have.
Early Assessment Program
Early Start Program


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Real Estate Management and Development
Company Overview of Lincoln Property Company
BOARD MEMBERS AFFILIATED WITH Tim Byrne *
President and Chief Executive Officer of Residential Division
MOST CONNECTED PEOPLE TO Tim Byrne
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To contact Lincoln Property Company, please visit . Company data is provided by Capital IQ. Please use this form to report any data issues.
Our data partners will research the update request and update the information on this page if necessary. Research and follow-up could take several weeks. If you have questions, you can contact them at email@example.com.


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Carbohydrate Addicts Diet VS. Atkins
Hello All. I am trying to get the pros and cons of these two "Diets." One is atkins induction which is less than 20 net carbs a day and the other is The Carb Addicts Diet which means no carbs all day except one hour a day you can eat whatever you would like. I have been sticking mainly to Atkins and occasionally eating an hours worth on the weekends, but I am wondering if I should consider the other. I feel icky and grumpy a lot on atkins and get frusterated by my own special requests for low carb foods all the time. I really like the idea of having an hour to eat what I would like. I wouldn't go crazy, and I would be health concious during that hour, but I would still like to lose around 10 pounds a month. Does anyone have any input on this?
You'll only know by trying it.
I recall years ago when CA first appeared. It seemed great, but I happen to be particularly sensitive to carbs, and a plan like that would never work for me.
However, everyone is different in terms of their toleration for carbs. I know that one of the authors of CA lost about 80 lbs easily eating this way, so it can work.
Whether it can work for you is something you'll only know if you try it.
It sounds like on both you will have special requests or modifications when you're eating out in public. Personally, I can do A LOT of damage in an hour, I couldn't be trusted on that.
Good luck with what you decide!
I think it sounds like a possible fit for you! I think the best plan is the one a person can stick to longterm .. and it sounds like CAD might help that. Being grumpy on Atkins is not going to keep you going .. I have been doing this since 2003 and there is no way in hell I'd have been able to take it off and keep it off if i was not relatively happy with the weightloss portion of that food plan ..
Honestly, when you go to maintenance and try to keep that weightloss, you do not eat all that differently from the weightloss portion .. that is something that is hard to see when a person is trying to just shed the pounds. I think you are being very very wise looking for something that is manageable for yourself!
Personal Opinion: I'd just try to stick very rigorously to the rules of the plan, time-wise, etc, do the zero carb thing suring the day but do not make it prison fare or you'll overdo it at your 1-hour meal.
Let us know how you do if you do decide to go that route! I have always thought it sounded like a really really good plan.
Hi, Tia, (I refuse to call such a beautiful young woman Tubby Girl)!
I tried the CA for a few years back.
It was ugly.
and It was embarrassing.
I had no control.
toward the end I just ate ice cream and what the hour turned out to be was a daily binge.
HOWEVER, you seem to be really aware of exactly what is going on with you.
That is powerful.
I say try it, see how you like it and how it likes you!
I will be stalking you for updates!
I admire your insights.
I can't imagine it works for very many people. The whole point is, is that a way to deal with an addiction? Let's say we are talking to alcoholics. would it seem like good advice that they could drink anything they wanted one hour a day? I didn't think so.
the science of weight gain and insulin metabolism and all has come a long way since then, and I don't think there is any scientific basis for the idea it's ok to eat carbs during a one hour window. in fact, it's clearly better to spread your carbs over the day to avoid that huge insulin spike that's dead set on storing as much of what you eat as fat as it can!
if you want to eat more carbs than Atkins starts with, I suggest you get through induction and work through the rungs of OWL to see what you can and can't eat without gaining more weight.
the problem is, from the perspective of a MUCH older person who has lost, regained, lost, regained more, over and over... the problem is to find something you can stick with. better to stay at 250 the rest of your life than to be saying the same thing you are now, but substituting 350 as your current weight, 10 or 20 years from now. it happens, believe me.
I can also do *a lot* of damage in an hour and my blood sugar would spike into the 400's with that kind of carb load.
I think if you're looking to keep the carbs in your diet, there are much better alternatives (e.g. South Beach).
The plan is NOT to eat gorge yourself for an hour - that's like saying JUDDD is eat 4000 calories every other day and lose weight. It's common sense too. You can gain w/Atkins if you say "well you don't have to count calories so I'll 4000 calories a day w/zero carb"...it's suppose to be a moderate carb meal to reward yourself. It works for ppl like me who don't have binge issues and dont' like the restriction of "never" and "for the rest of my life".
I know ppl for whom it has worked great.
I think the 1 hr. carb-ier meal is supposed to be controlled. Divide your plate in thirds, consisting of veggie, salad and carbs. Go back for seconds, but only if you have seconds of everything. At least that is how I remember it.
If I eat more than 45gm of carbs a day I'm in trouble with sugar spikes and on the CAD, there are easily *way* more than that in just one helping. Some might say, well then limit those carbs to what I can tolerate. Yep...but then that's Atkins. ;)
u will never know unless u try it.
there are quite a number of plans out there involving some sort of carb restriction, not all are as austere as ATKINS phase I. I always recommend Living Low Carb (revised edition 2010)by Johnny Bowden. One chapter in it discusses in detail 38 different plans, most of them involve some sort of carb restriction. Best of luck. Love & Profits: FLATFERENGHI
If this diet works, are there forums specifically dedicated to it, to discuss and promote it, by people who use this diet or WOE long term?
I haven't read the diet, but I don't see how this would be any different than people who eat thier whole days worth of food in one sitting, even if they are doing LC.
The problems that I see; that you should verify are explained away by the diet include:
(a) The amount of insulin that is released in response to glucose entering into your blood stream, will be more than minimal, and will trigger the storage of fats in your blood stream, and will halt the flow of fats flowing out of you fat cells.
(b) This may kick you into and out of ketosis on a daily basis or so depending on how many carbs you handle to remain in keto. Normally when going into keto, you loose a lot of water, and vitamins and minerals along with it. If you are going in an out repeatedly, I imagine you would have to watch your water and sodium/magnesium/potassium/calcium baances carefully?
It's a wonderful plan! Try it out! :)
I tried it once and freaked out on it, eating too much at night. It was a loooong time ago. As I remember it, you were supposed to eat a "normal" meal that would last no longer than one hour. I did OK for a few days then I started eating more and more each night. My stomach felt full, but each night was less satisfying than the night before.
I'm not saying I don't agree with the principal of pushing the main insulin release to the evening meal. I think that is a fantastic idea, especially since my blood sugar is higher in the morning. The CA plan was just too liberal for me.
Thanks everyone! I need to read the book. I am just curious if the CAD and other similar diets like South Beach help you to lose as quick as Atkins. I really want to lose 10 a month which really isn't that quick. I'm curious if you are in ketosis or if the cravings are low too. I am pretty good at not doing a lot of damage. I don't really like junk food like cake/icecream chips, because I know it hurts my belly. But I would love to have some whole wheat pasta sometimes at night and FRUIITT in the summer!!
I lost about 8 lbs the first week and 2-3 lbs a week after that.
CAD/CALP's great plan unless you turn your RM into a full on binge or can't stop.....
There are some peop on that thread who've been very successful. If you google you'll find some on other discussion forums.
South Beach is also allows more carbs and is a very popular plan w huge success.
It is whatever works for you and what you can live with.
Not everyone has rapid weight loss w Atkins.
I used to follow CAD. Actually I lost 100 pounds doing that. I loved it and found that I had less bouts of cheating on my plan as if I really wanted something I could have it. The only reason I've gone away from it is b/c I wanted to try something different. I do plan on it being my maintenance plan in the future.
The thing is that after a few weeks I did stop the cravings for the chocolate cake and the huge portions of sweets, but I always knew that if I wanted real pizza or to have a bowl of cereal or something I could.
i've tried CAD before and while i can be fairly high in carbs (in comparison to other lc'ers, not in comparison to the SAD) and stay in ketosis, not everyone is like this. fruit is something you could enjoy on most lc plans, whole wheat pasta, no. but how about dreamfields? it's excellent. there are a LOT of choices out there for you :cool:
"The problems that I see; that you should verify are explained away by the diet include:
(a) The amount of insulin that is released in response to glucose entering into your blood stream, will be more than minimal, and will trigger the storage of fats in your blood stream, and will halt the flow of fats flowing out of you fat cells. "
I first learned about managing insulin release when I read the Hellers' Healthy for Life, which outlines an eating plan similar to CAD.
I LOVE this plan. You do have to control yourself but its a sense of relief for me knowing I can have a little bit of "x" for dinner. I keep my portions in check and stick to the plan. I do advise NO cheat day since you kind of get one every night at dinner :) I do highly recommend this plan.Especially if youre in college or tend to go out a lot with friends. Pretty soon you'll find yourself choosing more low carb options for dinner than you realized. Hope this helps!! Ive had great success with this plan! Good luck to you!
I only know one person CA worked for in the last decade or so. Everyone else didn't lose or gained that I personally know who tried it. The one success was a woman with serious self control, she really budgeted for protein, and her one meal would be EXACTLY balanced as they recommend NOT a free for all. Once a week she had a happy meal with a diet drink. It worked for her.
Definite failure for me without staying in ketosis and avoiding all binge triggers.
If I were you, I would pick your plan based upon what you can sustain for the longterm as I think the differences in weightloss amounts are not **that** different ... imho, all the plans work if you work them.
I tried CAD before I started Atkins and it did not work for me. The plan is a good plan, but I am a carb addict and the reward dinner was not moderate for me at all. I would overdo it.
Atkins is better for me and once I got past induction, I felt very comfortable and not deprived.
I think trying CAD would be good if you are not someone who has problems with controlling your eating during a meal like the reward meal. If I could do it, I probably would.
Thank you all so much. I love this site and all its members. Such good information to be gathered here. I think I would do very well not binging on my diet, but I would have to work to include the proteins and all the other rules that go along with this diet. I am going to grab the book and keep you all updated. Thanks again.
Lately I see so many people (not just here) complaining about how slow they are losing. Many of those people are losing regularly and average 1 - 2 lbs a week. I don't remember years ago so many people thinking that was slow, but constantly hear that complaint lately. It makes me wonder if shows like Biggest Loser where the contestants lose large amounts of weight because they are focused 24/7 only on losing weight is the reason. I know the people in real life that complain about it all the time, are all Biggest Loser Fans. I keep trying to reassure them that as long as they are losing they are doing good, and shouldn't expect big results every week.
Over on the 'other plans' there is CAD/CALP thread. Terri (Hoppin) is w/in a few pounds of goal. She stayed w it spedifically because she could do it for life.
She has linked to her site which has pics and she is truly an inspiration. She also feels that she has gained better control w CALP.
Probably one of the big upsides is that for those who have family that don't follow lc eating plan, the meal that is shared can fit right into the reward meal.
I have done it before with success. I liked it but I found I invariably went off the plan after a time. I could not seem to stick to it. If I am in weight loss mode, it is one of the occasional tools I will employ while low-carbing (say, if I know I'm going to visit folks for a meal), besides intermittent fasting (which just means having a window of 5 to 6 hours a day where I will eat and the rest of the time abstain). The thing I disliked the most was that it was only 1 hour one could eat. Yikes! When I prepare food, I tend to nibble. Oh boy, this made things tough!
That was my experience but I've heard of several other people that have lost 100 pounds or more (even someone on this thread) with CALP and kept if off with the same plan. Amazing to me.
Hello -- I initially lost 121 pounds using CALP, a version of CAD that emphasizes a balanced Reward Meal. It's a great plan -- it works! And I found it very easy to follow. It took me about 21 months to lose the weight. However, I am disheartened to say that within the last 8 months, I have gained about 35 pounds back (this is the first time I have said this on this forum), and this is a topic I'd like to post about in the main forum, as I really have been searching for help. But back to CAD/CALP -- it's a great, do-able plan! Good luck!
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Holiday Inn Express Newport Beach
Holiday Inn Express Newport Beach in Newport Beach
Holiday Inn Express Newport Beach
Hotel Guest Rating: 7.8/10
2300 West Coast Highway
Newport Beach, CA 92663
Welcome to the Holiday Inn Express Newport Beach
Free Wi-Fi, complimentary breakfast and an outdoor pool are among the perks guests find at the non-smoking Holiday Inn Express Newport Beach, set in a neighborhood of shops, restaurants and nightlife.
Hotel Features
The non-smoking Holiday Inn hosts 64 rooms on two floors and underwent a renovation in 2012. All accommodations feature flat-panel TVs, free Wi-Fi, coffeemakers, microwaves, mini-fridges, work desks and beds with premium linens. Each morning's breakfast is on the house, as are weekday newspapers. Road warriors are happy to know that business services such as faxing are available. After a day spent touring the area, working or driving, leisure guests make a beeline for the outdoor pool and fitness room. Parking is available on-site.
Hotel Location
The Holiday Inn Express is 30 minutes from Disneyland and five miles from Fashion Island Mall. The Catalina Island Ferry departs three miles from the hotel, and the Newport Beach boardwalk and bike trail are just a few steps from the front door. John Wayne Orange County Airport is eight miles away.
Guest Favorites
Priceline guests like the "convenient" location of Holiday Inn Express Newport Beach, which is within steps of the Newport Beach boardwalk.
Holiday Inn Express Newport Beach Amenities
- Accessible facilities
- Air conditioning individually controlled in room
- Buffet breakfast
- Business center
- Coffee/Tea maker
- Color television
- Complimentary breakfast
- Desk with lamp
- Dry cleaning
- Fitness center on-site
- Hairdryer
- High speed internet access for laptop in public areas
- High speed internet connection
- Housekeeping - daily
- Housekeeping - weekly
- Ice machine
- Interior corridors
- Ironing board
- Late check-out available
- Meal included - continental breakfast
- Meeting rooms
- Microwave
- Mini-refrigerator
- Non-smoking
- On-site business center
- On-Site parking
- Onsite laundry
- Outdoor pool
- Parking
- Premium movie channels
- Private bathroom
- Public area air conditioned
- Safe deposit box
- Satellite television
- Separate closet
- Spare electrical outlet available at desk
- Speaker phone
- Stereo
- Telephone jack adaptor available
- Two-line phone
- Valet same day dry cleaning
- Voice mail
- Wireless connectivity
- Wireless internet connection
- Wireless internet connection in public areas
Hotel Information
Upon check-in photo identification and credit card are required. All special requests are subject to availability upon check-in. Special requests cannot be guaranteed and may incur additional charges. Guests are required to show a photo identification and credit card upon check-in. Please note that all Special Requests are subject to availability and additional charges may apply.
Hotel Guest Reviews of the Holiday Inn Express Newport BeachOur hotel ratings and reviews are from real hotel guests. Priceline.com ensures that its reviews are guests-only by proactively sending hotel surveys to customers after they've completed their hotel stays. In the post-stay surveys, priceline.com hotel customers are asked a number of questions about their stay and the hotel. On a scale of 1-10 with 10 being the best, the survey asks guests to rate their overall experience and specifically rate the hotel's cleanliness, staff and location. Priceline.com does not allow site visitors to post unsolicited hotel reviews.
June 27, 2014
The location was perfect.
June 14, 2014
Solo Traveler
This guest did not leave comments about this hotel.
March 27, 2014
Family Traveling with Young Children
This guest did not leave comments about this hotel.
March 4, 2014
Solo Traveler
January 22, 2014
Solo Traveler
January 5, 2014
Family Traveling with Young Children
This guest did not leave comments about this hotel.
November 26, 2013
October 2, 2013
Group Traveler
This hotel was great! My second time I stay at a Holiday Inn Express and I would really recommend them! The hotel is clean and staff is friendly! Other reviews mentioned a sewer smell... I did smell it but the smell was only outside. And I don't think the smell is caused by the hotel. My family and I went walking to Starbucks in the morning and on the way there we smelled the same thing by another location off the street. It's a stench that arises occasionally because of the surrounding waters! ...
September 24, 2013
Business Traveler
Don't stay here. You'll regret it. The odor is absolutely toxic.
August 26, 2013
Family Traveling with Young Children
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Search Results
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iFixIt tears down the original Mac 128k
In honor of the Mac turning 30, the teardown experts at iFixIt took it upon themselves to tear open the original Mac daddy, the Mac 128k.
They even put together this clever and '80s-themed teardown/review video.
Now given that Apple today does all it can to keep tinkerers from prying open its devices, from iMacs to iPhones, you may be surprised to hear that the original Mac received a reparability score of 7 out of 10 (with 10 being the easiest to repair).
By way of contrast, the iPad Air has a laughably low repairability score of 2. Apple's late-2012 iMac, meanwhile, has a repairability score of 3.
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Find synonyms Find exact match
Disclosures: Carol A Kauffman, MD Nothing to disclose. Kieren A Marr, MD Grant/Research/Clinical Trial Support: Pfizer [Antifungals (Voriconazole, anidulafungin)]; Astellas [Transplant infections (Liposomal amphotericin B, micafungin, isavuconazole)]. Consultant/Advisory Boards: Astellas [Antifungals (Liposomal amphotericin B, micafungin, isavuconazole)]; Merck [Antifungals (Posaconazole)]; Cidara Therapeutics [Antifungals (Antifungals)]; Chimerix Therapeutics [Antivirals (Antivirals)]. Patent Holder: MycoMed Technologies [Aspergillosis (Fungal diagnostics)]. Equity Ownership/Stock Options: MycoMed Technologies [Aspergillosis (Fungal diagnostics)]. Anna R Thorner, MD Employee of UpToDate, Inc.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence.
INTRODUCTION — The term candidemia describes the presence of Candida species in the blood. Candidemia is the most common manifestations of invasive candidiasis. Candida in a blood culture should never be viewed as a contaminant and should always prompt a search for the source of the bloodstream infection. For many patients, candidemia is a manifestation of invasive candidiasis that could have originated in a variety of organs, whereas for others, candidemia originated from an infected indwelling intravenous catheter [1].
The treatment of candidemia in adults will be reviewed here. The epidemiology, pathogenesis, clinical manifestations, and diagnosis of candidemia are discussed separately; an overview of Candida infections and the management of other forms of invasive candidiasis are also presented elsewhere. (See "Epidemiology and pathogenesis of candidemia in adults" and "Clinical manifestations and diagnosis of candidemia and invasive candidiasis in adults" and "Overview of Candida infections" and "Candida endocarditis" and "Chronic disseminated candidiasis (hepatosplenic candidiasis)" and "Candida infections of the central nervous system" and "Candida osteoarticular infections".)
The treatment of candidemia in neonates and children is discussed in detail separately. (See "Treatment of Candida infection in neonates" and "Candidemia in children: Treatment".)
Antifungal susceptibility testing is also reviewed separately. (See "Antifungal susceptibility testing".)
EPIDEMIOLOGY — C. albicans is the most common cause of candidemia, but there has been increased isolation of non-albicans species of Candida in recent years. Most prominent have been C. glabrata and C. parapsilosis, followed by C. tropicalis and C. krusei. This is important because some C. glabrata isolates are resistant to fluconazole, and all C. krusei isolates are resistant to fluconazole (table 1). In addition, the minimal inhibitory concentrations for C. parapsilosis with all the echinocandins are higher than for other Candida species. Risk factors for infection with fluconazole-resistant Candida species include neutropenia, recent azole use, and others. The epidemiology of candidemia is discussed in detail separately. (See "Epidemiology and pathogenesis of candidemia in adults", section on 'Prevalence of Candida species'.)
ANTIFUNGAL AGENTS — Therapeutic antifungal classes for the treatment of candidiasis include the polyenes, azoles, and echinocandins. The relative advantages and disadvantages of available agents are discussed in this section. Efficacy is discussed below. (See 'Azoles' below and 'Echinocandins' below and 'Amphotericin B' below.)
Azoles — Fluconazole has been widely used for the treatment of candidiasis since its approval by the US Food and Drug Administration (FDA) in 1990. The azoles work primarily by inhibiting the cytochrome P450-dependent enzyme lanosterol 14-alpha-demethylase [2]. This enzyme is necessary for the conversion of lanosterol to ergosterol, a vital component of the cellular membrane of fungi. General susceptibility patterns of Candida species to fluconazole and other antifungal agents are shown in the Table (table 1).
Fluconazole has an excellent safety profile and is available in intravenous and oral formulations and is also inexpensive, since it is now generic. Fluconazole is highly bioavailable, making oral dosing appropriate for most patients. Most trials evaluating the efficacy of fluconazole for candidemia have used 400 or 800 mg [3-6]. For candidemia, we recommend that fluconazole be dosed as follows: 800 mg (12 mg/kg) loading dose, then 400 mg (6 mg/kg) orally daily [7].
Other available azoles include voriconazole, posaconazole, and itraconazole:
●The activity of voriconazole against Candida species is superior to that of fluconazole, with minimal inhibitory concentrations (MICs) that are a log or more less than fluconazole [8]. However, cross-resistance between fluconazole and voriconazole is seen frequently, especially with C. glabrata. Voriconazole has significantly greater in vitro activity against C. krusei isolates compared with fluconazole because of more effective binding of its cytochrome P450 isoenzyme [9]. (See "Antifungal susceptibility testing", section on 'Azoles' and "Antifungal susceptibility testing", section on 'Azoles'.)
●Posaconazole is available only as an oral suspension. It is approved for use as a prophylactic agent for fungal infections in allogeneic hematopoietic cell transplant recipients with graft-versus-host disease and in patients with prolonged neutropenia due to chemotherapy for hematologic malignancies. It is also approved for oropharyngeal candidiasis but not for systemic candidiasis. (See "Prophylaxis of invasive fungal infections in adult hematopoietic cell transplant recipients" and "Prophylaxis of invasive fungal infections in adults with hematologic malignancies" and "Treatment of oropharyngeal and esophageal candidiasis".)
●Itraconazole is sometimes used for mucosal candidiasis but is not used for systemic infections.
Azoles interact with multiple different cytochrome P450 enzymes; alternative antifungal agents, such as echinocandins, may be preferred if patients are taking other medications that utilize P450 pathways. (See "Pharmacology of azoles", section on 'Drug interactions'.)
The pharmacology of the azoles is discussed in detail elsewhere. (See "Pharmacology of azoles".)
Echinocandins — The echinocandins include caspofungin, anidulafungin, and micafungin. Echinocandins are noncompetitive inhibitors of the synthesis of 1,3-beta-D-glucan, which is an integral component of the fungal cell wall [10]. They have excellent activity against most Candida species, have favorable toxicity profiles, and are approved for the treatment of candidemia and other forms of invasive candidiasis. The echinocandins are preferred over azoles for the initial treatment of candidemia if C. glabrata or C. krusei is identified or suspected [11].
Due to their broad-spectrum activity against Candida species, the echinocandins are used extensively for candidemia and invasive candidiasis. The highest echinocandin MICs are found for C. parapsilosis and C. guilliermondii. Resistance to echinocandins has been noted in only a few individual cases until recently. However, acquired resistance has been increasingly reported, especially in C. glabrata. The mechanism of echinocandin resistance is similar in all species and involves mutations in the FKS 1 or FKS 2 genes that control the enzyme targeted by the echinocandins.
The echinocandins are administered intravenously as follows:
●Caspofungin is given at an initial dose of 70 mg on the first day of treatment, followed by 50 mg daily; dose reduction is required with hepatic dysfunction.
●Anidulafungin is given at an initial dose of 200 mg on the first day, followed by 100 mg daily.
●Micafungin is given at a dose of 100 mg daily for candidemia; no loading dose is needed.
Adverse effects of all echinocandins are generally mild and include fever, thrombophlebitis, headache, and elevated aminotransferases [11]. The pharmacology of the echinocandins is discussed in detail separately. (See "Pharmacology of echinocandins".)
Amphotericin B — Amphotericin B is a polyene antifungal agent that disrupts fungal cell wall synthesis because of its ability to bind to sterols, primarily ergosterol, which leads to the formation of pores that allow leakage of cellular components. Amphotericin B deoxycholate, which was the standard drug for the treatment of candidiasis for decades, demonstrates rapidly cidal in vitro activity against most species of Candida. It is also associated with significant nephrotoxicity. This has led to the development of various lipid-based derivatives, including liposomal amphotericin B and amphotericin B lipid complex (ABLC). A third formulation, amphotericin B colloidal dispersion (ABCD) is used infrequently, in part because it causes more infusion-related reactions than amphotericin B deoxycholate. These lipid-based compounds have much less toxicity than amphotericin deoxycholate but are significantly more expensive. (See "Pharmacology of amphotericin B" and "Amphotericin B nephrotoxicity".)
The recommended doses for candidemia follow [7]:
●Lipid formulations of amphotericin B – 3 to 5 mg/kg intravenously daily
●Amphotericin B deoxycholate – 0.5 to 1 mg/kg intravenously daily
SUSCEPTIBILITY PATTERNS — Susceptibility testing for Candida species is becoming more readily available and widely used. General susceptibility patterns are shown in the Table (table 1), and general patterns for each class of antifungal agent are discussed above. (See 'Amphotericin B' above and 'Azoles' above and 'Echinocandins' above.)
Specific drug resistance information for the various Candida species is found below. Antifungal susceptibility testing is discussed in greater detail separately. (See "Antifungal susceptibility testing".)
C. albicans — The incidence of C. albicans resistance is extremely low. An analysis of in vitro susceptibilities of approximately 90,000 isolates of C. albicans collected from 40 countries from 1997 to 2005 demonstrated that only 1.5 percent were resistant to fluconazole [12]. Individual cases and small series of non-mucosal infection with fluconazole-resistant C. albicans have been reported from several tertiary care centers and usually occur in immunosuppressed patients who are taking fluconazole chronically for prophylaxis [13-15].
Most C. albicans isolates are susceptible to the echinocandins, although resistance has been reported [16,17]. The vast majority of C. albicans isolates are susceptible to amphotericin B.
C. krusei — C. krusei is intrinsically resistant to fluconazole due to an altered cytochrome P450 isoenzyme [18]. This resistance cannot be overcome with use of higher drug doses. Voriconazole binds more effectively to the cytochrome P450 isoenzyme in C. krusei than fluconazole, resulting in higher rates of susceptibility [19].
There are geographic differences in the incidence of voriconazole resistance. In an international surveillance study that included nearly 3500 bloodstream isolates of C. krusei, 83 percent of isolates were susceptible to voriconazole, ranging from 75 percent in Latin America to 92 percent in North America [20]. C. krusei isolates are usually susceptible to posaconazole [21].
In the large surveillance study described above, all C. krusei isolates were susceptible to the echinocandins (caspofungin, micafungin, and anidulafungin) [20]. However, individual cases of resistance to the echinocandins have been reported [22-24].
C. krusei demonstrates decreased susceptibility to amphotericin B, requiring higher doses (1 mg/kg daily of amphotericin B deoxycholate or 5 mg/kg daily of lipid-based formulations) to be used for treatment. C. krusei is usually resistant to flucytosine.
C. glabrata — Many C. glabrata isolates are resistant to the azoles, mostly due to changes in drug efflux [7,25]. This type of resistance can sometimes be overcome by using higher doses of fluconazole. Cross-resistance among the azoles is common with C. glabrata. Among the Candida species, the MICs for voriconazole are highest with C. glabrata. Isolates that are resistant to fluconazole are generally resistant to voriconazole as well [26,27].
The echinocandins have generally retained excellent activity against C. glabrata, although isolated cases of resistance have been reported [28-32].
Of note, there is increasing concern that some C. glabrata bloodstream isolates with resistance to fluconazole and voriconazole can also become resistant to the echinocandins. In a surveillance study of the in vitro susceptibility of 1669 C. glabrata bloodstream isolates collected in the United States between 2006 and 2010, 162 isolates (9.7 percent) were resistant to fluconazole, of which 98.8 percent were also not susceptible to voriconazole and 9.3, 9.3, and 8.0 percent were resistant to anidulafungin, caspofungin, and micafungin, respectively [27]. The mechanisms of fluconazole and voriconazole resistance are similar and largely mediated by efflux pumps that can export all azoles [33]. In addition, it was noted that of 162 isolates that were resistant to fluconazole, 18 (11.1 percent) were also resistant to one or more of the echinocandins, with associated mutations in FKS1 or FKS2 genes [27]. In comparison, there were no echinocandin-resistant strains detected among 110 fluconazole-resistant C. glabrata isolates tested between 2001 and 2004, years in which echinocandins were used sparingly. It is not clear what impact these findings will have on treatment regimens for candidemia.
A 10-year study of C. glabrata bloodstream infections at a single medical center in the United States showed an increase in echinocandin resistance from 4.9 percent in 2001 to 12.3 percent in 2010 [34]. This resistance was confirmed by the presence of FKS mutations; strains categorized as susceptible did not possess acquired mutations. On multivariate analysis, echinocandin resistance was associated with prior exposure to an echinocandin. Among 78 fluconazole-resistant isolates, 11 (14.1 percent) were resistant to one or more echinocandins and 8 (10.3 percent) were resistant to all echinocandins.
Amphotericin B has delayed killing kinetics against C. glabrata in vitro [35]; higher doses of amphotericin B are recommended when treating known C. glabrata infection (1 mg/kg daily of amphotericin B deoxycholate or 5 mg/kg daily of lipid-based formulations).
C. parapsilosis — C. parapsilosis is highly susceptible to most antifungal agents. An international surveillance study of 9371 C. parapsilosis isolates collected between 2001 and 2005 found high rates of susceptibility to fluconazole (91 to 96 percent) and voriconazole (95 to 98 percent) in all geographic regions except Africa and the Middle East (79 and 86 percent susceptible to fluconazole and voriconazole, respectively) [36].
The minimal inhibitory concentrations for C. parapsilosis with all the echinocandins are higher than for other Candida species [25]. The clinical implications of these in vitro data are unclear. In an analysis of five trials of caspofungin use in patients with invasive candidiasis, the overall (clinical and microbiologic) success rate among patients with C. parapsilosis (74 percent) was similar to patients with invasive candidiasis caused by other Candida species [37]. A multicenter prospective observational study of candidemia due to C. parapsilosis in Spain found no differences in outcomes of patients who were treated with an echinocandin compared with those who were treated with an azole [38]. These results should be interpreted with caution because this was not a randomized trial; it is unlikely that such a study will be performed [39].
C. tropicalis — C. tropicalis is usually susceptible to the azoles, amphotericin B, and the echinocandins. However, breakthrough C. tropicalis bloodstream infections with resistance to caspofungin have been reported rarely in patients with hematologic malignancies [17,40,41].
C. lusitaniae — C. lusitaniae is unique among Candida species in that it is often resistant to or quickly becomes resistant to amphotericin B; however, it is usually susceptible to the azoles and echinocandins [42].
C. guilliermondii — C. guilliermondii is an uncommon Candida species that in some studies has appeared to cause infections more often in patients who have hematologic malignancies [43]. Treatment can be problematic because some isolates have reduced susceptibility to fluconazole and many have reduced susceptibility to echinocandins [44]. However, C. guilliermondii is usually susceptible to amphotericin B.
C. dubliniensis — C. dubliniensis shares many phenotypic traits with C. albicans, and many isolates were previously misidentified as C. albicans. Special techniques must be undertaken in the microbiology laboratory to differentiate between these two species [45]. C. dubliniensis rose to importance in the mid-1990s when it was found primarily in AIDS patients and most of the isolates were fluconazole resistant. It has subsequently been shown that this species causes disease in other populations as well, and the susceptibilities are similar to those of C. albicans. Most C. dubliniensis isolates are azole susceptible and can therefore be treated with fluconazole; they are also susceptible to echinocandins and amphotericin B.
APPROACH TO ANTIFUNGAL THERAPY — The most common antifungal agents used currently for the treatment of candidemia are fluconazole and the echinocandins (caspofungin, micafungin, anidulafungin). Formulations of amphotericin B are given less often due to the risk of toxicity. Both the echinocandins and the azoles are better tolerated than amphotericin B formulations [46].
In all cases, candidemia requires treatment with an antifungal agent [7]; it should never be assumed that removal of a catheter alone is adequate therapy for candidemia. Several studies have noted the high mortality rates associated with candidemia [47-49] and have shown that mortality is highest in those patients who were not treated with an antifungal drug [48,49]. Furthermore, prompt initiation of therapy is crucial. (See 'Catheter removal' below and 'Outcomes' below.)
Choice of initial agent — When choosing an antifungal agent in patients with suspected candidemia, the following factors should be considered [7]:
●History of recent azole exposure
●Prevalence of different Candida species and current antifungal susceptibility data in the clinical unit and medical center
●Severity of illness
●Relevant comorbidities that increase the risk of fluconazole-resistant Candida species (eg, neutropenia) (see "Epidemiology and pathogenesis of candidemia in adults")
●Evidence of involvement of the central nervous system, cardiac valves, eyes, and/or visceral organs
●History of intolerance to an antifungal agent
It is particularly important to determine the risk of fluconazole-resistant Candida isolates, such as C. glabrata and C. krusei (see 'C. glabrata and C. krusei' below).
Nonneutropenic patients — In nonneutropenic patients with candidemia who are clinically stable, who have not been exposed to recent azole therapy, and who are in clinical units or medical centers in which C. glabrata or C. krusei are uncommonly isolated (<15 percent of all species causing candidemia), we suggest initial therapy with fluconazole rather than an echinocandin (table 2) [7]. (See 'Azoles' below.)
In nonneutropenic patients with moderately severe or severe infections and/or who are at increased risk of C. glabrata or C. krusei infection, we favor an echinocandin (caspofungin, micafungin, or anidulafungin) and we would not use fluconazole as initial therapy, prior to the identification of the causative species [7]. However, in patients who have documented C. glabrata infection, who are already improving clinically on fluconazole or voriconazole, and whose follow-up blood cultures are negative, continuing with the azole is reasonable. (See 'C. glabrata and C. krusei' below and 'Echinocandins' above.)
Neutropenic patients — In patients who are neutropenic, there are several important considerations in choosing appropriate therapy for candidemia [7]:
●Most neutropenic patients with candidemia should be treated with an echinocandin or an amphotericin B formulation. Azole drugs have not been studied extensively for treatment of candidemia in this population. Also, neutropenic patients who are heavily pretreated with azole drugs as part of prophylactic regimens are at increased risk for fluconazole-resistant Candida spp, such as C. glabrata and C. krusei (table 2). If amphotericin B is used, a lipid formulation is preferred. (See 'C. glabrata and C. krusei' below and 'Echinocandins' above and 'Amphotericin B' above.)
●Fluconazole should be restricted to clinically stable patients who have not received recent azole prophylaxis. (See 'Amphotericin B' above and 'Azoles' above and 'Echinocandins' above.)
C. parapsilosis — Patients with candidemia caused by C. parapsilosis should be treated with fluconazole rather than an echinocandin [7]. However, for patients with C. parapsilosis who are already improving clinically on an echinocandin and whose follow-up blood cultures are negative, continuing with the echinocandin is reasonable. (See 'C. parapsilosis' above.)
C. glabrata and C. krusei — A difficult issue is which antifungal agent to use when C. glabrata is isolated from the blood [7]. Because many C. glabrata strains are resistant to fluconazole, the most conservative approach is to treat fungemia due to this species with an agent other than fluconazole. However, several studies that used fluconazole found no differences in outcome related to the species causing candidemia [3,50,51]. In a study in cancer patients, C. glabrata bloodstream infection responded less well to therapy than C. albicans, but neither the initial regimen nor the species of Candida was an independent predictor of poor outcome [52]. Nevertheless, based on in vitro data, it is prudent to avoid use of fluconazole for the initial treatment of C. glabrata. (See 'C. glabrata' above.)
Since C. krusei is intrinsically resistant to fluconazole, this agent is avoided when C. krusei is suspected. (See 'C. krusei' above.)
Because of its safety profile, an echinocandin is generally preferred over amphotericin B for treatment of candidemia due to C. glabrata and C. krusei. Voriconazole is also approved for this indication, but there is likely to be cross-resistance between fluconazole and voriconazole among C. glabrata isolates. This cross-resistance does not occur with C. krusei. In clinical units or medical centers in which C. glabrata or C. krusei are commonly isolated (defined as >15 percent of all species causing candidemia), we suggest using an echinocandin rather than fluconazole for empiric therapy until the species is known. There are few differences among the echinocandins, and any of the three approved agents (caspofungin, micafungin, anidulafungin) can be used when indicated. (See 'Echinocandins' above.)
Some studies have shown increased rates of echinocandin resistance among C. glabrata bloodstream isolates. Resistance should be suspected in patients who have received echinocandins in the recent past and in patients who develop candidemia while receiving an echinocandin for prophylaxis or empiric therapy (eg, for neutropenic fever); in these situations, an amphotericin B formulation should be used until antifungal susceptibility testing results are available. (See 'C. glabrata' above.)
Candida krusei is usually susceptible to echinocandins and voriconazole but is uniformly resistant to fluconazole. These isolates can also demonstrate high minimum inhibitory concentrations (MICs) to amphotericin B, and, for this reason, higher doses of this drug should be used for C. krusei infection (1 mg/kg daily of amphotericin B deoxycholate or 5 mg/kg daily of lipid-based formulations). We prefer lipid formulations of amphotericin B to amphotericin B deoxycholate because the lipid formulations have fewer toxicities. (See 'Amphotericin B' above.)
Dosing — The dosing of fluconazole, the echinocandins, and amphotericin B formulations is discussed above. (See 'Azoles' above and 'Echinocandins' above and 'Amphotericin B' above.)
Oral step-down therapy — Nonneutropenic patients with Candida isolates likely to be fluconazole susceptible (eg, C. albicans) or proven to be fluconazole susceptible by antifungal susceptibility testing who are clinically stable can be switched from an echinocandin to fluconazole [7]. (See "Antifungal susceptibility testing".)
Voriconazole is recommended as oral step-down therapy only for patients with C. krusei or voriconazole-susceptible C. glabrata [7]. For other Candida isolates, it does not offer a clear advantage compared with fluconazole.
Duration — The appropriate duration of therapy for candidemia has not been studied. A minimum of two weeks of therapy after blood cultures become negative has been used in most clinical trials and is the recommended duration in the 2009 Infectious Diseases Society of America (IDSA) guidelines [7]. Daily blood cultures should be performed after initiating therapy in order to determine the date of sterilization. If blood cultures remain positive, then a search for a metastatic focus, such as an abscess or endocarditis, must be undertaken. In addition, all patients should have resolution of symptoms attributable to candidemia and resolution of neutropenia (eg, absolute neutrophil count >500 cells/microL and showing a consistent increasing trend) before antifungal therapy is discontinued [7]. (See "Overview of neutropenic fever syndromes", section on 'Neutropenia' and "Treatment of neutropenic fever syndromes in adults with hematologic malignancies and hematopoietic cell transplant recipients (high-risk patients)", section on 'Duration'.)
A longer duration of therapy and consultation with an infectious disease specialist are warranted in patients who have metastatic foci of infection or endocarditis. (See "Treatment of endogenous endophthalmitis due to Candida species" and "Candida osteoarticular infections" and "Candida endocarditis" and "Chronic disseminated candidiasis (hepatosplenic candidiasis)".)
Combination therapy — Whether more than one antifungal agent should be used together for the treatment of candidemia has not been established, although combination therapy is generally not given for the treatment of candidemia.
A controlled trial randomly assigned 219 nonneutropenic patients with candidemia to fluconazole (800 mg/day) alone for two weeks or fluconazole (800 mg/day) plus amphotericin B (0.7 mg/kg per day) for the first four to seven days followed by fluconazole alone to finish the two-week course [6]. There was more rapid clearing of fungemia with initial combination therapy, but the success rates overall were similar in the two groups.
Evidence — Several randomized trials have shown that fluconazole is as effective as amphotericin B for the treatment of candidemia in immunocompetent patients [3-5,53]. The echinocandins appear to be as effective as and better tolerated than amphotericin B formulations and, in one study, more effective than fluconazole [54-57]. The majority of patients in these studies were not neutropenic.
Data are more limited in neutropenic patients with candidemia. No randomized trials have been adequately powered to evaluate the efficacy of antifungal therapy in neutropenic patients [7], and data are derived from small subset analyses of randomized trials, open-label studies, and retrospective studies [5,54,55,58-60]. Based upon the widespread use of fluconazole prophylaxis in neutropenic patients and the resulting increased prevalence of non-albicans Candida species with reduced susceptibility to fluconazole, most neutropenic patients with candidemia are treated with an echinocandin or an amphotericin B formulation. (See 'Neutropenic patients' above.)
Azoles — Several large randomized trials have shown that fluconazole is as effective as amphotericin B for the treatment of candidemia in immunocompetent patients [3-5,53].
In a randomized trial, fluconazole was compared with anidulafungin for treatment of invasive candidiasis in 245 patients: 89 percent had candidemia and only 3 percent were neutropenic [56]. The combined clinical and microbiologic response rates were significantly higher in patients assigned to the anidulafungin arm both at the end of therapy (74 versus 57 percent) and at two-week follow-up (65 versus 49 percent). Mortality rates at 60 days were similar.
The effectiveness of voriconazole for candidemia was shown in a randomized trial in nonneutropenic patients who were treated with either voriconazole alone or amphotericin B for three to seven days followed by fluconazole [61]. Voriconazole therapy led to sterilization of the bloodstream as rapidly as sequential therapy. Success rates at the end of treatment (66 percent for voriconazole and 71 percent for sequential therapy) were similar to those noted in previous trials with other antifungal regimens for the treatment of candidemia. The clinical role for voriconazole in comparison with echinocandins remains unclear. A major concern is the cross-resistance to voriconazole that is seen among many isolates of C. glabrata that are fluconazole resistant. (See 'C. glabrata' above and 'C. glabrata and C. krusei' above.)
Echinocandins — Several randomized trials have compared the efficacy of echinocandins with either an amphotericin B formulation or fluconazole among patients with invasive candidiasis [54-57]. The majority of patients had candidemia and were not neutropenic.
The echinocandins appear to be as effective as and better tolerated than amphotericin B formulations and, in one study, more effective than fluconazole as illustrated by the following observations:
●In one randomized trial, caspofungin was shown to be equivalent in efficacy to amphotericin B [54]. Patients were randomly assigned to the two different treatment arms controlling for neutropenia and APACHE II scores. In an analysis that excluded patients who did not have a documented infection or received less than one day of the treatment drug, the two drugs demonstrated equivalent efficacy (73 percent for caspofungin versus 62 percent for amphotericin B). Caspofungin was associated with less toxicity.
●A randomized multinational noninferiority trial compared micafungin to liposomal amphotericin B [55]. In a modified intent-to-treat analysis, success rates for clinical and microbiologic cure were similar (74 and 70 percent for micafungin and liposomal amphotericin B, respectively). Micafungin was associated with fewer adverse events. In a later subset analysis of only those patients who had infection with C. glabrata or C. krusei, outcomes were similar between those receiving micafungin and those receiving liposomal amphotericin B [57].
●In another randomized trial, anidulafungin resulted in superior combined clinical and microbiologic response compared with fluconazole (65 versus 49 percent at two-week follow-up), although 60-day mortality rates were similar, as discussed above [56]. (See 'Azoles' above.)
Data are more limited in neutropenic patients with candidemia compared with nonneutropenic patients. Efficacy data for the echinocandins in neutropenic patients comes from small subset analyses of randomized trials and open-label studies [54,55,58,59]. Although the efficacy of the echinocandins in neutropenic patients cannot be firmly established based upon these studies, the response rates to the echinocandins appear to be similar to or better than formulations of amphotericin B.
A separate issue is the relative efficacy of the different echinocandins. This was addressed in a randomized trial of adults with candidemia and other forms of invasive candidiasis that compared two doses of micafungin (100 mg or 150 mg daily) with one another and with caspofungin (70 mg once followed by 50 mg daily) [58]. The lower dose of micafungin was equivalent to both the higher dose of micafungin and to caspofungin.
In a later subset analysis of only those patients who had infection with C. glabrata or C. krusei, outcomes were similar among the three treatment groups [57]. In another trial, two different doses of caspofungin (70 mg once followed by 50 mg daily versus 150 mg daily) were compared in patients being treated for invasive candidiasis [62]. Similar rates of mortality (at eight weeks) and significant adverse effects were observed between the groups.
Amphotericin B — Amphotericin B formulations have been proven to be effective in several randomized trials [3-5,53] (see 'Azoles' above). However, amphotericin B formulations are often avoided due to their increased toxicity compared with azoles and echinocandins. They remain useful in cases when resistance to the other antifungal classes is suspected or proven.
Comparison of trial data — A 2008 meta-analysis of 15 randomized trials compared different antifungal agents for the treatment of invasive candidiasis and found that there were no differences in mortality between fluconazole and amphotericin B or the echinocandins [46]. However, there was a higher rate of microbiologic failure in patients who received fluconazole compared with amphotericin B (relative risk [RR] 1.52; 95% CI 1.12-2.07) or the echinocandin anidulafungin (RR 2.0; 95% CI 1.16-3.44).
A 2012 patient-level quantitative review evaluated observational data gathered from 1915 patients included in seven randomized treatment trials of candidemia and invasive candidiasis, including those described above [63]. Patients who were treated with an echinocandin had improved survival compared with those treated with an azole or an amphotericin B formulation (odds ratio 0.65, 95% CI 0.45-0.94).
OPHTHALMOLOGIC EVALUATION — All patients who have candidemia, whether or not they have ocular symptoms, should undergo an ophthalmologic examination by an ophthalmologist to look for evidence of endophthalmitis, as recommended in the Infectious Diseases Society of America (IDSA) guidelines for treatment of candidiasis [7]. (See "Epidemiology, clinical manifestations, and diagnosis of fungal endophthalmitis", section on 'Ophthalmic examination'.)
CATHETER REMOVAL — Central intravenous catheters should be removed in patients with candidemia [7,64]. Clearance of fungemia occurs more quickly when catheters are removed [65,66], and higher mortality has been documented if catheters remain [38,48,63,66-68]. In addition, treatment with an antifungal agent is required [7]; it should never be assumed that removal of a catheter alone is adequate therapy for candidemia.
Some authorities have suggested that catheter removal may not be necessary in neutropenic patients with candidemia (eg, patients with hematologic malignancies undergoing cytotoxic chemotherapy, hematopoietic cell transplant recipients with graft-versus-host disease), in whom the source is often the gastrointestinal tract rather than the central venous catheter [69,70]. Some clinicians will attempt to retain the catheters in such patients [71,72]. An extension of this argument, put forth by the same authors, is that not all catheters have to be removed in nonneutropenic patients with candidemia [69].
Several studies, albeit with limitations, have evaluated whether central venous catheter removal is beneficial:
●A retrospective subgroup analysis of two randomized trials of patients with candidemia was performed in order to assess the potential benefit of early central venous catheter removal [70]. In the univariate analysis, early removal of the central venous catheter (within 24 or 48 hours) did not improve time to mycologic eradication or rates of persistent of recurrent candidemia but was associated with improved treatment success and survival. However, in the multivariate analysis, these benefits were lost.
●A study in cancer patients used a fivefold difference in quantitative cultures taken from the central catheter and a peripheral vein to help define catheter-associated candidemia [73]. Using these criteria, patients with non-catheter sources did not benefit from catheter removal in addition to antifungal agents.
●In contrast to the studies described above, an individual patient-level quantitative review that evaluated observational data gathered from seven randomized treatment trials of candidemia and invasive candidiasis found that removal of a central venous catheter was associated with decreased mortality (odds ratio 0.50, 95% CI 0.35-0.72) [63].
There are multiple limitations to observational studies and subgroup analyses of randomized trials, including unrecognized confounders, treatment bias, lack of standardized criteria for catheter removal or data on time to removal, and lack of statistical power [74,75]. Despite the controversy, the current consensus, including that noted by the Infectious Diseases Society of America (IDSA) guidelines, remains that in most patients with candidemia, intravascular catheters should be removed, realizing that in some patients this may not be feasible [7,64-66,74,76].
EMPIRIC ANTIFUNGAL THERAPY — Empiric antifungal therapy is given routinely to patients with neutropenic fever since they are at substantial risk for invasive candidiasis. This is discussed in detail separately. (See "Treatment of neutropenic fever syndromes in adults with hematologic malignancies and hematopoietic cell transplant recipients (high-risk patients)", section on 'Addition of an antifungal agent'.)
In addition, nonneutropenic patients who have persistent fever or unexplained hypotension despite broad-spectrum antibacterial agents may have candidemia or invasive candidiasis. These patients may benefit from early empiric or preemptive therapy with an antifungal agent. The choice of agent should be guided by the hemodynamic stability of the patient and whether the patient has a history of prior exposure to antifungal agents [77]. If the etiologic agent has not been identified, the approach to empiric therapy will be influenced by whether the patient is known to be colonized with resistant Candida species and the proportion of candidemias due to resistant species within a particular medical center or patient unit. (See "Epidemiology and pathogenesis of candidemia in adults", section on 'Risk factors'.)
The 2009 Infectious Diseases Society of America (IDSA) guidelines recommend that empiric antifungal therapy should be considered in critically ill patients who are at risk for invasive candidiasis and who have persistent fevers despite antibacterial therapy (table 2) [7]. Criteria for the need for empiric therapy remain poorly defined and should include the clinical assessment of risk factors (eg, central venous catheters, total parenteral nutrition, hemodialysis, trauma, broad-spectrum antibiotics, recent surgery [particularly abdominal surgery]), serologic markers for invasive candidiasis (eg, beta-D-glucan), if available, and culture data regarding Candida colonization at nonsterile sites. (See "Epidemiology and pathogenesis of candidemia in adults", section on 'Risk factors'.)
It is not clear whether the empiric use of fluconazole is beneficial. One multicenter randomized trial in the intensive care unit (ICU) setting found no difference in rate of invasive candidiasis or outcomes between patients given fluconazole empirically and those given placebo; invasive candidiasis occurred in only nine patients in the fluconazole group and in 11 patients in the placebo group (5 versus 9 percent), a nonsignificant difference [78]. However, this trial was underpowered, with so few patients developing invasive candidiasis that a significant treatment benefit could not be shown.
We emphasize that empiric antifungal therapy should be given only to patients who are thought to be at substantial risk of invasive candidiasis. In such patients, we favor therapy with either an echinocandin or fluconazole, depending upon the risk of resistant Candida species. (See "Epidemiology and pathogenesis of candidemia in adults", section on 'Risk factors' and 'Choice of initial agent' above.)
PROPHYLAXIS IN ICU PATIENTS — Because mortality remains high in patients with candidemia, antifungal prophylaxis has been studied as a means to prevent its occurrence. However, the optimal approach remains unclear. Currently, there are no recommendations for antifungal prophylaxis among intensive care unit (ICU) patients [7]. We suggest not routinely using prophylactic antifungal agents in the ICU setting. However, consideration can be given to the use of prophylaxis in selected patients in ICUs that have high rates (>5 percent) of invasive candidiasis. Only patients at the highest risk for invasive disease should be targeted for prophylaxis; risk factors include central venous catheters, parenteral nutrition, hemodialysis, trauma, broad-spectrum antibiotics, and recent surgery (particularly abdominal surgery) (see "Epidemiology and pathogenesis of candidemia in adults"). In such patients, either an echinocandin or fluconazole can be used, depending upon the risk of resistant Candida species.
Broad use of fluconazole in an ICU setting has been shown to decrease invasive candidiasis in several trials [79,80]. However, most ICUs have not adopted routine fluconazole prophylaxis because widespread use would likely contribute to increasing fluconazole resistance. In a small study, more selective fluconazole prophylaxis for patients at high risk for intraabdominal candidiasis was beneficial [81]. At least four meta-analyses have been published on the subject of antifungal prophylaxis in the ICU setting [82-85]. All four noted a reduction in invasive candidiasis, but only one showed a reduction in mortality (risk ratio 0.60, 95% CI 0.45-0.81) [82].
Two studies assessed the efficacy of caspofungin prophylaxis in the ICU setting. A small prospective observational study found that caspofungin prevented intraabdominal candidiasis [86]. In a randomized trial, adults who were deemed to be at high risk for invasive candidiasis (by utilizing a clinical prediction rule) were randomly assigned to receive caspofungin or placebo; there was a trend toward disease reduction in the caspofungin arm [87]. There were 10 Candida infections in 102 patients in the caspofungin arm and 14 in the 84 patients who received placebo, a nonsignificant difference. There were no differences in mortality between the two groups.
OUTCOMES — Untreated candidemia has a mortality rate of over 60 percent [47]. With treatment, the overall mortality of candidemia is approximately 30 to 40 percent [63,75]. A delay in treatment can increase mortality [88-90]. In one retrospective cohort study of 230 patients with candidemia, the number of days that passed from notification of the first positive culture for yeast to the initiation of fluconazole correlated with increased mortality rates as follows: day 0 (15 percent); day 1 (24 percent); day 2 (37 percent); day 3 (41 percent) [88].
Among candidemic patients with septic shock, the outcomes are even poorer. In a retrospective cohort study of hospitalized patients with septic shock and a positive blood culture for Candida spp, 155 of 224 patients (64 percent) died during hospitalization [91]. The in-hospital mortality rate among the 142 patients who had adequate source control within 24 hours of the onset of septic shock and antifungal therapy administered within 24 hours of the onset of septic shock was 53 percent, compared with 98 percent among the 82 patients for whom these goals were not attained. On multivariate analysis, both failure to achieve timely source control (adjusted odds ratio [aOR] 77.4, 95% CI 21.5-278.4) and delayed antifungal therapy (aOR 33.8, 95% CI 9.7-118.0) were highly associated with in-hospital mortality. Other factors that were independently associated with in-hospital mortality on multivariate analysis included red blood cell transfusion, solid tumor with metastases, class IV congestive heart failure, and higher APACHE II score.
Factors that have been associated with increased mortality in other studies of hospitalized patients with candidemia include higher APACHE II scores, inadequate fluconazole dosing, retention of a central venous catheter, increasing age, use of immunosuppressive therapy, and infection with C. tropicalis [63,67,92]. C. parapsilosis has been associated with lower mortality rates than other Candida species [63]. In ICU patients, diabetes mellitus, immunosuppression, and mechanical ventilation were associated with death in one study [93], whereas, in non-ICU patients, glucocorticoid use at the time that a positive blood culture was drawn was associated with increased mortality in another study [67].
Among cancer patients, persistent neutropenia, higher APACHE III score, and visceral dissemination have been associated with poor prognosis [71].
●The choice of antifungal therapy for invasive candidiasis, including candidemia, depends upon a variety of factors including history of recent azole exposure; prevalence of different Candida species and current antifungal susceptibility data in the clinical unit and medical center; severity of illness; relevant comorbidities (eg, neutropenia, recent abdominal surgery); evidence of involvement of the central nervous system, cardiac valves, eyes, and/or visceral organs; and history of intolerance to an antifungal agent. (See 'Choice of initial agent' above.)
●For nonneutropenic patients with candidemia who are clinically stable, who have not been exposed to recent azole therapy, and who are in clinical units or medical centers in which C. glabrata or C. krusei are uncommonly isolated (<15 percent of all species causing candidemia), we suggest fluconazole rather than an echinocandin (Grade 2B). We also suggest fluconazole for the uncommon neutropenic patients who meet these criteria (Grade 2B). The usual dose of fluconazole is an 800 mg loading dose followed by 400 mg orally daily. (See 'Nonneutropenic patients' above and 'Neutropenic patients' above.)
●For nonneutropenic and neutropenic patients with candidemia who are clinically unstable or in patients who have risks for infection with azole-resistant organisms, such as with prior drug exposure, we suggest an echinocandin (caspofungin, micafungin, anidulafungin) rather than fluconazole for initial therapy (Grade 2B). For patients at risk for echinocandin resistance (eg, prior recent exposure to an echinocandin), an amphotericin B formulation should be used until antifungal susceptibility testing results are available. Treatment can be changed to fluconazole (or an echinocandin) if the isolate is found to be susceptible. (See 'C. glabrata and C. krusei' above and 'Choice of initial agent' above.)
●The echinocandins are administered intravenously as follows:
•Caspofungin is given at an initial dose of 70 mg on the first day of treatment, followed by 50 mg daily; dose reduction is required with hepatic dysfunction.
•Anidulafungin is given at an initial dose of 200 mg on the first day, followed by 100 mg daily.
•Micafungin is given at a dose of 100 mg daily for candidemia; no loading dose is needed. (See 'Echinocandins' above.)
●Blood cultures should be checked daily after initiating antifungal therapy until they become negative. (See 'Duration' above.)
●All patients who have candidemia, whether or not they have ocular symptoms, should undergo an ophthalmologic examination by an ophthalmologist to look for evidence of endophthalmitis. (See 'Ophthalmologic evaluation' above.)
●In the patient with candidemia alone, treatment should be continued for 14 days after blood cultures have yielded no yeast. In addition, all patients should have resolution of symptoms attributable to candidemia and resolution of neutropenia before antifungal therapy is discontinued. Patients with candidemia and metastatic foci of infection (eg, eye, bone, heart, liver, spleen) require a longer duration of therapy. (See 'Duration' above and "Treatment of endogenous endophthalmitis due to Candida species" and "Candida osteoarticular infections" and "Candida endocarditis" and "Chronic disseminated candidiasis (hepatosplenic candidiasis)".)
●Central intravenous catheters should be removed in patients with candidemia, when feasible. However, catheter removal is controversial in neutropenic patients, in whom the gastrointestinal tract is often the source. Some clinicians will attempt to retain the catheter in these patients. (See 'Catheter removal' above.)
●Empiric antifungal therapy recommendations in patients with neutropenic fever are discussed in detail elsewhere. (See "Treatment of neutropenic fever syndromes in adults with hematologic malignancies and hematopoietic cell transplant recipients (high-risk patients)", section on 'Addition of an antifungal agent'.)
●We suggest not giving empiric antifungal therapy to most patients in the intensive care unit (ICU) (Grade 2B). However, this approach, using either an echinocandin or fluconazole, is reasonable in a subset of high-risk ICU patients who have all of the following characteristics:
•Persistent fever despite broad-spectrum antibiotics
•Risk factors for invasive candidiasis
•Positive serologic markers for invasive candidiasis and/or isolation of Candida from multiple nonsterile sites (see 'Empiric antifungal therapy' above)
●We suggest not routinely using prophylactic antifungal agents in the ICU setting (Grade 2C); it is reasonable to give antifungal prophylaxis with either an echinocandin or fluconazole to high-risk patients in ICUs in which the incidence of invasive candidiasis is >5 percent. (See 'Prophylaxis in ICU patients' above.)
All topics are updated as new information becomes available. Our peer review process typically takes one to six weeks depending on the issue.


text:
Kinda see I was wanting to try steeping the grains like sun tea . I thought It would give it different. Characteristics to the flavor . Am i right since it would take a few days to steep . I was going to try it this weekend. Cause here in NJ its going to be like 90 all weekend
I think you will be surprised at what would be growing in your 'grain tea' after a couple days in the sun....
Well it would be sealed. Plus I was going to boil the water first before I added anything to it. To kill any bacteria.
To my knowledge that's a way to start a sasion...having the sweet wort and grains be in contact with the elements would either cause a wild fermentation or a sour wort beer.
Grain goes funky REALLY quick. Leave some spent grain out for 24 hours sometime in a "sealed" container...yuck. Smells like rotten milk.
I wouldn't try it, but if you do, do it with very little and see what happens.
_________________________________Skal! Den Faaborg Bryggeri
What's a session?
Even with a sealed container..having wet grain in a Luke warm bucket for a cooked days will allow the grain to mold. That's why they dry grain after malting