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Because myeloma develops in the bone marrow, almost everyone with advanced stage multiple myeloma will develop bone complications. In this program, you'll learn about the most up-to-date treatments for these bone complications from hemotalogist Dr. Paul Richardson of Dana Farber Cancer Institute, and you'll hear about the experiences of Mike Katz, a vice president of the International Myeloma Foundation who is living with myeloma.
Welcome to this HealthTalk webcast. Before we begin, we remind you that the opinions expressed on this webcast are solely the views of our guests. They are not necessarily the views of HealthTalk, our sponsors or any outside organization. And, as always, please consult your own physician for the medical advice most appropriate for you.
This program is produced by HealthTalk and sponsored through an unrestricted educational grant from Novartis Oncology.
Dick Foley:
The symptoms of multiple myeloma are not always obvious and can easily be mistaken for signs of other conditions. The doctor who first saw business consultant Mike Katz about his hip pain diagnosed the problem as sciatica, an inflammation of the sciatic nerve. It was months before Mike learned that he had a massive tumor in his pelvis - the result of the myeloma he didn't even know he had. By then, his bones were already in bad shape. We'll be hearing from Mike in a moment, and we'll also be talking with Dr. Paul Richardson, a myeloma specialist from the Dana Farber Cancer Center [Institute] in Boston about the critical connection between myeloma and your bones.
And now our first guest is Mike Katz, a management consultant for Booz Allen Hamilton, specializing in information technology and e-commerce, and vice president of the International Myeloma Foundation. Mike, welcome to our program.
Mike Katz:
Thank you.
Can you tell us more about your personal story with myeloma and your original diagnosis?
The world changed substantially for me back in 1990 when an orthopedist finally discovered that what we thought was a common case of sciatica was actually a massive, plasmacytoma in my pelvis. The tumor had destroyed much of what's called the iliac crest, the top back part of the pelvis. But, fortunately, I was able to find a very skilled surgeon who cut out the diseased bone and replaced it with a bone graft that allowed me, basically, to get back to normal.
I was diagnosed with multiple myeloma - a fairly uncommon kind called nonsecretory, which meant that I had no blood or urine protein to measure, which is part of why it took so long to diagnose. I also had something called focal disease, meaning that it showed up in very specific spots so that bone marrow biopsies are also pretty useless in trying to monitor the disease. So, for the long term, managing the disease has been a challenge of coming up with different ways to catch it before it sneaks up on you.
And the original symptom was pain?
Yes, pain. I got off a long flight to Hong Kong on a business trip and suddenly found myself limping for no apparent reason.
Tell us how your disease and approaches to this disease have changed over the past 15 years, and the treatments you have tried at different points.
At the beginning, the disease was very much limited to individual locations. We were able to treat it with surgery and radiation focused on specific lesions, specific spots where there was bone damage starting to occur. Over the years, it's gotten to be a bit more aggressive and diffuse and shows up in more places, so we've had to use various drugs, steroids, some chemotherapy and most recently, thalidomide and dexamethasone to keep it under control.
The other thing that's changed dramatically over the years is that there are a lot more treatments available, and there [are] also many more techniques for monitoring the disease. At the beginning, I had a lot of trouble because of the lack of indicators, just finding problems early enough before damage would occur. Now we have new tests. The Freelite test is able to measure disease activity in a lot of nonsecretory patients, including myself, and new imaging technology like PET/CT scans detect the disease through a whole body scan and find out where the disease might be causing bone issues. So it's become a lot easier to monitor the disease over the years, even though it's gotten more aggressive. And there are many more treatments now available.
In terms of those treatments, you've tried them all: radiation, surgery, chemo and the newer forms of treatment?
I haven't tried them all, but I've tried quite a few of them.
How have you tolerated all those treatments?
I've been pretty lucky. I've been able to keep working and have a fairly active personal life and also do a lot of volunteer work in the myeloma community. I've been very fortunate in that the treatments have worked and the side effects have not been terribly onerous.
I guess that would explain the way you've been able to manage a fairly typical family and work life over these years despite dealing with this disease.
One of the things I've always tried to do is keep too busy to be sick, and if you can get away with that health-wise, that seems to be a smart strategy for managing a disease like this.
Were there ever real low points where you just didn't feel you could function?
Of course. When I was originally diagnosed, the surgery was pretty cataclysmic. I was hospitalized for a couple of weeks. And there was a skull tumor that got out of hand at one point that put me out of commission for a couple of weeks. There have been occasions where I haven't been at my best, but have struggled through just for the sake of struggling through. We have a choice, but I think my choice is to keep moving forward and to try and minimize the disease as much as possible, and [for] other patients [who] I've dealt with, that seems to be a winning strategy. I always tell people to push themselves. Don't do anything stupid but don't get into the trap of, I don't feel good so I don't want to do anything. That's just a vicious cycle. It gets worse and worse.
It sounds like you have made some admirable choices, and we appreciate hearing your story, Mike. We'll get back to you in a bit.
I want to introduce Dr. Paul Richardson, who is a myeloma specialist at Dana Farber Cancer Institute at Harvard Medical School in Boston, Massachusetts. He's a researcher in the department of medical oncology and hematologic malignancies. Welcome, Dr. Richardson.
Dr. Paul Richardson:
Thanks so much for having me.
Perhaps you could start by telling us about your research and the clinical work you do related specifically to myeloma and bone complications.
Dr. Richardson:
As you heard so nicely from Mike, myeloma intrinsically is a disease that affects the bone, so it's a primary target for the activity of the disease. Our research here at Dana Farber is very much focused on targeting the micro-environment, the neighborhood within which the myeloma likes to live and grow. That involves the bone marrow stroma, which is this sort of media in which the myeloma cells grow, and of course the adjacent bone matrix that surrounds that as well.
So our new therapies are targeted not just at the myeloma itself, but also on the neighborhood within which the myeloma is nestled and grows and can destroy bone as part of that process. As you heard from Mike, that can be a very challenging thing to deal with, and a lot of our treatments, by treating the myeloma help with the bone issues.
We have a whole armamentarium of drugs that we use to tackle myeloma now fortunately, [and] we have certain cornerstones of treatment of bone complications. These include the drugs we call the bisphosphonates, which are very specific and work directly on the bone. But a lot of our other treatments, which work on the neighborhood of the myeloma as well, help indirectly, on the bone, by virtue of targeting the myeloma itself.
In our research here at Dana Farber, inspired and led by my chief, Dr. Kenneth Anderson, and our fantastic laboratory program and a superb clinical program, is targeted at trying to develop these new treatments in ways which are less toxic to patients, more specific against their cancer and, therefore, more effective.
We know that myeloma is a plasma cell disease that has its origins in the bone marrow, but maybe you can help us understand precisely what happens to someone like Mike, whose myeloma revealed itself as tumors in various bones in different parts of his body.
Dr. Richardson:
Basically, plasma cells are a very important part of how we normally deal with infection. These are cells that produce antibodies in response to infection. They are highly sophisticated cells derived from what we call B cells or B lymphocytes. Normally, they begin their life in the lymph nodes and travel into the bone marrow.
What happens when they go a little wrong, or go significantly wrong as happens in myeloma, is that they go out to these "neighborhoods" but they take them over. In Mike's case, you heard how his disease actually presented with destruction of bone. That happens because the myeloma secretes growth factors and cytokines that directly stimulate the activation of things called osteoclasts. These are normal cells within the bone, but when they're stimulated, they break bone down. And if they are overstimulated, they break down too much bone. They create the lytic holes that we see in bones caused directly by the effects of myeloma. Conversely, there is some recent evidence to show that myeloma not only stimulates these osteoclasts to attack the bone and destroy bone so it can set up shop in the space it so created, but it can also suppress osteoblasts - cells that in the normal bone actually build bone.
So myeloma does two things. It both stimulates the osteoclasts to destroy bone and, at the same time, it may suppress osteoblasts to prevent the normal regeneration of bone. As a result of that, bone is destroyed, becoming thinner and weaker - what we call osteoporosis. That leads to bone pain, which is a very frequent presenting symptom of myeloma, as you heard from Mike, and these holes, these lytic lesions in the bone evolve.
The most commonly affected bones are typically in the back [and] in the hips and pelvis. But we also see involvement of the extremities, in particular the upper and lower extremities - the femur and the humeri, which are the upper parts of the legs and the upper parts of the arm. This is very important because these can be prone to fracture. Other key areas that the myeloma can involve are the ribs. The ribs can be uncomfortable in patients who do have bony involvement and their sternum [breastbone].
It's very challenging when the bony involvement of the spine can be advanced, because that can not only lead to back pain, but can also damage the spinal cord. Bony lesions can affect the skull as well. Sometimes they don't cause any symptoms at all in the skull, but occasionally they can damage key areas of bone that can lead to symptoms affecting cranial nerves or areas of the sinuses and facial bones.
One important complication to mention about bony involvement from myeloma is that when you destroy bone, you release calcium into the bloodstream. That is a significant potential complication of myeloma, which we call hypercalcemia, which means too much calcium in the blood. That's a very important complication to avoid because when it does occur, it can make patients feel extremely unwell, and it can also cause kidney damage and various effects on other organ systems.
Mike mentioned he did have a skull tumor. That is somewhat rare, is that right?
Dr. Richardson:
Absolutely. In the natural history of this illness in years gone by, unfortunately, most patients did not live very long. The typical survival was three years. Now with newer treatments, people are living much longer, which is great news. The thing is, some of the presentations that were described as rare in the past, affecting the skull and the face, can now change because people are living with their disease for much longer.
In Mike's case, for 14 years.
Dr. Richardson:
Exactly, which is wonderful. And having the pleasure of meeting Mike and seeing how well he is and how well he looks, frankly, when I first met him, I wouldn't have thought he was ill at all, he looked so good. But I think that's a great credit to him, but at the same time, also a great credit to the new treatments.
I think it's not just a matter of treatment, it's also the new diagnostics and keeping on top of the disease, because a lot of the issue with bone complications is when things go and are not treated because we don't know they are happening.
Dr. Richardson:
That's an extremely good point, Mike. Obviously, we are much more trained and experienced in the management of bony complications. I have the privilege of working with a very good orthopedic team who were specifically interested in bony complications, and that helps me a great deal. Mike, you're absolutely right. With the advent of new scanning techniques and better radiology, MRI [magnetic resonance imaging] being more widely used and CT [computed tomography] imaging with bone windows, we're that much better at evaluating and managing bone disease.
Just as Mike described, we have many patients in our practice who have lived with their disease for many years when they would not have been expected to based upon how things stood a number of years ago.
Dr. Richardson:
I think it's worth spending a little time on treatments for bone disease. There are treatments that we use now that changed the management of bone disease, and probably the most important of them are the bisphosphonates. These are intravenous medicines given typically every three to four weeks, and they work by switching off these osteoclasts, which are the cells that destroy bones when they are stimulated. Bisphosphonates, very specifically, target these osteoclasts and turn them off. The other thing that they do as part of that process is keep the calcium under control. They have been clearly shown in clinical trials to improve the quality of life for patients by reducing bony complications, fracture risk, and very importantly, can help the pain.
Do most patients tolerate them pretty well, and would you say this is now the standard therapy for bony disease with myeloma?
Dr. Richardson:
It's absolutely the standard of care. Because we don't know exactly how long to treat bone complications with these drugs, we tend to treat continuously. We have to be very careful because there can be some complications from them. They are relatively uncommon, but they need to be watched for.
Generally speaking, patients tolerate bisphosphonates well. The first infusion can be complicated by a flu-like syndrome that may occur afterwards. We think this is because bisphosphonates work on very stimulated cells and cause changes in cytokines and, consequently with the first few infusions, patients can report aches and pains in their joints and low-grade temperatures. Obviously, that should be reported to your doctor, but at the same time, that's a complication that can be readily managed with simple analgesics and things that can bring your temperature down like Tylenol. That infusional syndrome around bisphosphonates typically passes over several administrations and isn't repeated with subsequent ones.
More challenging complications can occur, but again, they are relatively uncommon. A very important one for patients to know about [is that] bisphosphonates can cause kidney damage. If it's watched for carefully, it can not only be anticipated early, but also by dose modification or stopping treatment for a few months, the process can be completely reversed and treatment can then restart and continue. That's not always the case, but obviously working closely with your treating physician would be very important in that regard.
There are two major bisphosphonates that we use. One is called pamidronate disodium, or Aredia, which is the older bisphosphonate that's given by a two hour infusion and has generally been well tolerated in clinical trials and in subsequent experience, although it can sometimes cause this kidney problem. The kidney problem is characterized by the production of too much albumin in the urine, and the lab tests that monitors kidney function, the serum creatinine and the serum BUN, can elevate in that context. Usually, this can be readily reversed by simply holding the Aredia and then restarting it when the protein in the urine has disappeared or markedly reduced and the laboratory tests for the blood have returned to normal.
Zoledronic acid [Zometa] is a more potent bisphosphonate given intravenously as well. It's very active. It has the convenience to be given over a shorter period of time. Typically, at our center, we administer the drug over about 30 minutes, and it's very well-tolerated, similar to Aredia. It too can cause a renal problem, but the problem is a little different. It doesn't have quite the same mechanism that Aredia does, but it too can be anticipated by regular blood testing and making sure that patients are well-hydrated when they receive the drug. Again, if kidney damage does occur, provided it's picked up promptly, we withhold the drug and allow the kidneys to improve. Usually, patients can then go on to receive either additional zoledronic acid in the future or try Aredia as an alternative, if there's any concern. But generally speaking, both classes of bisphosphonates are well-tolerated.
I'm sure physicians are monitoring kidney function closely with all patients.
Dr. Richardson:
They should be, and they are certainly advised and educated to, but I think it's important for patients to look out for so that they can participate in their own care by bringing it to their caregivers' attention.
Mike, you said you've been taking bisphosphonates since the mid '90s. Were they always administered intravenously, and how long were your infusion sessions?
I've been taking Aredia since 1995, so I've had probably a hundred or more treatments. Originally, they were given in four-hour infusions, and then over the years we reduced it to two hours, and I get the drug every four weeks.
What about side effects for you, any problems that you've encountered?
Pretty much as Dr. Richardson said, the first few infusions I had some flu-like symptoms, which Tylenol did quite the job of controlling. Then after the third infusion, it was really nil effect at all that I could see.
Dr. Richardson, we've heard about one complication that affects the jaw. Should patients be alerted to that?
Dr. Richardson:
I'm so glad you mentioned that. There is this entity, osteonecrosis of the jaw. It's emerging as a complication of bisphosphonate administration, and I think [it] reflects the fact that bisphosphonates have been used for a long period of time now, successfully, in the management of bone complications from multiple myeloma and other cancers, such as breast cancer. Indeed, osteonecrosis has been reported in the jaw in patients taking bisphosphonates for osteoporosis. It is quite rare, and the reason I think it may occur is because there's a very high pressure between the teeth and the jaw and the bone. There's a very high pound-per-square-inch ratio there, and there may be some biologic effect that is not completely understood that triggers this complication.
But I don't know for sure. I do know it's an area of active research. Practically speaking, our advice to patients is to be very careful when they are having any kind of dental procedure to make sure that their dentist knows that they are on bisphosphonates and they monitor very carefully. Some of our dentists have recommended it. In fact, when our patients have any dental procedure, they actually take a break from their bisphosphonates at that time. That's been our tactical advice to patients based upon the reports that we've had so far, because there may be a relationship to infections and other trauma or other procedures going on in the jaw at around the same time.
Patients are at this point, with the medical community, trying to connect the dots here, because we don't really have the answers. So one of the things that has come up in support group meetings is that people don't often recognize the symptoms of osteonecrosis of the jaw. These are exposed bone in the mouth, bone spurs or bone erosion, and can be painful. It's not always picked up by the dentist as being that particular condition. One of the things that's very important for people to realize is that some of the initial cases that were diagnosed, people received surgical treatment and that actually can make the problem worse. If there's any suspicion that you have this problem, it's really important to get to a specialist and think before you move.
Thank you both for those alerts. We've been talking about intravenous or infused bisphosphonates so far. Are there oral bisphosphonates, doctor, and are those appropriate for myeloma patients?
Dr. Richardson:
There are oral bisphosphonates and they are given for osteoporosis of benign etiology, in other words, not associated with cancers. They are not as potent, generally speaking, as the intravenous bisphosphonates. So amongst our myeloma patients, it's not something we would routinely recommend, certainly in the United States. Having said that, in Europe, it is the practice among myeloma specialists there to give selected patients the oral bisphosphonate clodronate because they have seen activity from it, and it has the convenience of the oral route. In the U.S., we generally favor the bisphosphonates, which are given intravenously because they are that much more potent. And I think we all have an experience with them that has been relatively positive. Consequently, most people recommend the intravenous bisphosphonate.
You explained the mechanism of bisphosphonates - that they block the osteoblasts. Do they have the additional function of rebuilding bone that may have deteriorated somewhat?
Dr. Richardson:
That's a great question. Specifically, they inhibit osteoblasts and by so doing they allow osteoclastic activity to go ahead and rebuild bone. Interestingly, we don't usually see that with bisphosphonates alone. I think that's dependent on the success of other treatments for the myeloma and where bony remodeling has been seen, for example, [is] in the context of anti-myeloma therapy such as bone marrow transplant. Successful bone marrow transplant in the context of successful bisphosphonate use as well - that's where I'm aware of descriptions of bony remodeling occurring. But bone regrowth from bisphosphonates alone, I think, is not something we would expect.
Like many myeloma patients, Mike has been taking certain drugs to protect his bones and at the same time, he's taking other medications to control the myeloma. Do these combinations result in a better overall effect? And comment, if you would, on the safety of these drug combinations.
Dr. Richardson:
That very much depends on the drugs being used in conjunction with bisphosphonates. The good news with most of our new therapies with myeloma is that we've not seen interactions with bisphosphonates that have been harmful. There was a very important recent paper from a myeloma research group in Australia where they looked at the combination of thalidomide with zoledronic acid and showed no evidence there that this was a unique combination in which nephrotoxicity [kidney toxicity], for example, was enhanced. There had been some anecdotal reports that that might be the case, but this prospective trial effectively showed that not to be true. That's very reassuring to us. Basically, it would seem that these renal issues are independent and related to other events that may be occurring rather than due to the drug combination itself.
What's very true is that successful treatment of the myeloma with continued use of the bisphosphonates as part of supportive care, obviously, it's key to optimal patient management. And I think we've all been very encouraged that the use of drugs in conjunction with bisphosphonates has been relatively safe.
View a bone mets slide show
What else is now in the pipeline for treatment of myeloma-related bone disease or for earlier detection?
Dr. Richardson:
There are a whole host of things in bone disease that are important to note. There's a lot of basic science work that is targeting the receptors that are activated that trigger osteoclast activity. The so-called RANK ligand [is one], which offers opportunities for new drugs, such as osteoprotegerin, which is an antagonist of that and [is] currently under development. Newer variations of the osteoprotegerin are going forward in clinical trials.
We have the mainstay of the current potent bisphosphonates but at various levels, both preclinically and clinically, new agents for targeting bone disease are in the pipeline, and these will augment what we have already with the success of the bisphosphonates.
In addition to medical therapies that we've been discussing, are there other things that you can recommend for myeloma patients to do, to strengthen and protect their bones? Exercise comes to mind.
Dr. Richardson:
Absolutely, and I'll also look to Mike for advice here because he is very up-to-speed from the support groups as to what's helpful. I personally advise regular exercise that's low impact, walking obviously being very important.
There are numerous strategies now for intervening with specific bony complications. When I say numerous, perhaps that's too strong. But there are specific bone interventions that are being shown to be effective, such as, for compression fractures the use of kyphoplasty, which in my experience has really been helpful in patients in whom bone compression fractures can be an issue.
In terms of what patients can do, obviously being aware of the options that exist, being aware of the importance of regular exercise and mobility, and being aware of the importance of the standard supportive care such as bisphosphonates, would be key to enhancing their management of bone disease.
Calcium may be a questionable area. You mentioned the risk of excess calcium in the system.
Dr. Richardson:
I'll be very interested in Mike's view on this. I have to say, I do not regularly encourage patients to take extra calcium while they have a diagnosis of symptomatic, active myeloma with bone disease, because while bisphosphonates obviously reduce serum calcium in the face of hypercalcemia and work to inactivate osteoclasts, adding large amounts of calcium to that mix, I'm wary of. Someone with very bad osteoporosis in conjunction with bad bone disease, I'm aware of some colleagues who recommend small amounts of calcium being added. That may have some merit. I'm cautious about it because of the underlying process.
The bottom line is that patients need to have that dialogue with their doctor. There really isn't consensus on this, but I think we could all agree that adding large amounts of anything is a bad idea and adding anything without talking to the doctor, particularly when you are undergoing treatment, is always a bad idea.
Mike, tell us about your [approach] to exercise and also to nutrition.
I try not to do anything radical. I was able to keep up a regular exercise program until a couple of years ago when my original surgery started to wear out, [which was] sort of a consequence of long-term survivorship. But I am pretty active in terms of keeping mobile and walking and doing things like that. In fact, I just came back from a vacation in Italy where I was able to climb to the top of St. Peter's, which I'd done 30 years ago and really wanted to do again. So it's a bit of a personal victory.
[Are there] any dietary changes that have had a good, positive effect for you?
Well, I was putting on weight after I stopped exercising.
I went on the Atkins Diet, took off some pounds, and that actually improved the function of my hip - the problem I was having that took me out of the exercise program. Gaining weight is a problem that a lot of people have when you're taking steroids, and you're not feeling as well as you might feel. People tend to put on weight and that's never a great idea, but I try to advise people not to do anything crazy. People find all these miracle cures and miracle vitamins and want to take mega doses of things like vitamin C. Something that seems really innocent can interfere with treatment or just make you sick. So I always tell people they shouldn't do anything really radical. There's no magic bullet out there, and they should be talking to their doctor about these issues.
How about nutritional advice for your patients, Dr. Richardson?
Dr. Richardson:
I would echo what Mike said about being very careful and doing so in consultation with your caregiver. An important point you just mentioned, Mike, vitamin C at high dose[s]. Taking a high dose in someone with light-chain myeloma can actually be potentially hazardous because it can acidify the urine. Particularly, doses of vitamin C in excess of a gram can worsen kidney function, so I use that as an example of showing why what Mike says is so correct. Too much of anything, as a general rule, is to be avoided.
In terms of nutritional advice, I agree with Mike. One of the biggest challenges is steroids. They are tremendously burdensome to patients in terms of weight gain and metabolic abnormalities and the effects these metabolic abnormalities have on other aspects of quality of life, most importantly mood, fluctuations in blood sugar, and so forth. So we work very specifically with patients on nutrition depending on what treatment they are getting. For example, if they're on steroids, you want to avoid foods that are full of sugar and avoid concentrated sweets. In terms of other nutritional aspects, the healthy, balanced diet, in my experience [is best]. We've had some interesting, as yet anecdotal, experiences with supplements for neuropathies, which tend to be a big problem for us in some of our treatments. What we look at [is] the use of B complex folic acid in a multivitamin, again, not in excessive doses but in doses that may be helpful.
I wanted to give each of you of the opportunity to leave a final message with our audience. Perhaps we could start with you, Mike. [Is there] something you want to leave our audience with concerning your own experience with myeloma and bone disease?
I think that information is power, and I've devoted a substantial portion of my free time to working with the International Myeloma Foundation and getting out there and educating patients and patient seminars, support groups, Web sites, publications. I think the more people know, the better they are able to deal with the disease. And most of the time when people get into trouble, it's because of what they don't know. So, it's really important to learn about the disease, to learn what you need to do to monitor it, to treat it, and to prevent bone damage and other complications that can rob you of your quality of life. It's possible to live very well with multiple myeloma if you take an active role in managing it.
I'm glad you've mentioned support groups. For those who haven't located one, they might want to look at the benefits that flow to one through a support group. Thanks very much for that message.
Dr. Richardson, what final thoughts might you have for people living with bone complications of myeloma?
Dr. Richardson:
Mike put it very nicely. Indeed, information is power, and the good news is there are multiple options. There are very effective support groups, and the IMF is an outstanding example of one. There is the Multiple Myeloma Research Foundation as well.
In the context of bone complications, we've been very fortunate in that we've got some effective therapies, and there is more to come. I certainly recall, only too vividly, when I was just qualified, taking care of a patient with dreadful bony complications from myeloma and just being staggered at how powerless we were to help her. It's a complete night-and-day [change] now, and that's a tremendous tribute to the success of the new agents and therapies that we now have.
The proactive approach that Mike recommends is so important to harness the potential of these new drugs and established drugs, and in making quality of life and disease control and bone complications not unduly burdensome to patients.
Thanks to both of you for providing valuable information. We want to remind our listeners that we now have message boards where you can meet other HealthTalk members to talk about cancer and bone issues. Join in the conversation.
We've just had some great insights into the connection between myeloma and bone damage with Dr. Paul Richardson of Dana Farber Cancer Institute at Harvard Medical School and Mike Katz, a business consultant and vice president of the International Myeloma Foundation.
From our studios in Seattle and all of us at HealthTalk's Cancer Education Networks, I'm Dick Foley. We wish you and your families the best of health.


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With the Tourneo Courier, Ford has reverted to van-based underpinnings for its smallest MPV. Jonathan Crouch drives it.
Ten Second Review
Sometimes, something simpler is more sensible. Take the turn of the century trend to create small People Carriers with bespoke car-like design. All you actually need as a starting point for such a vehicle is a small van. And if you agree and happen to be looking for a very compact MPV, you might be interested in this one, the Ford Tourneo Courier.
Back in 2014, Ford launched its smallest-ever van, the Transit Courier. It was a design able to provide a perfect base for the creation of a supermini-sized People Carrier, but that option wasn't initially taken up because the Blue Oval brand already had one of those in its range, the Fiesta-based B-MAX. That car, launched in 2012 and notable for a clever design that completely dispensed with a central B-pillar, was ultimately a casualty of the market's fashion-led switch away from MPVs to SUVs and was quietly deleted in 2018.
Rather than replace it with something else styled from scratch, thoughts at Ford's design department turned back to the Transit Courier and its suitability as a base for a little People Carrier. Which is why we've got this car, the Tourneo Courier, launched in mid-2018 as part of a rejuvenated range of van-based Ford Tourneo People Movers. Despite the LCV underpinnings, there's no lack of sophistication here. Especially under the bonnet where family buyers choose between Ford's latest 1.5-litre EcoBlue diesel or a 1.0-litre EcoBoost petrol engine enhanced with cylinder deactivation.
Driving Experience
It's always quite refreshing to drive a car whose only purpose in life is to get from A to B as affordably as possible. So there are no pretensions here - no dynamic expectations that might be disappointed. Tourneo Courier buyers choose either a 1.5-litre EcoBlue diesel unit or the 1.0-litre three cylinder EcoBoost powerplant I tried. Both engines put out 100PS and must be mated to a freshly-designed 6-speed manual gearbox. The EcoBoost variant I tested will be the choice of most, who'll approve of the fact that this unit's efficiency has been enhanced by the additional of cylinder deactivation.
Ride quality over broken surfaces isn't as smooth as I'd like, but things settle down at highway speeds. At that point, the petrol engine's buzzy thrum subsides a little too, though you do still get quite a lot of wind and road noise from the boxy shape and the high profile tyres. As you'd expect from a car with such an expansive glass area, this MPV is simplicity itself to manoeuvre. The boxy shape makes it easy to see where the corners of the car are, the wide door mirrors are a commercial carry-over you'll be glad of and the expansive windscreen gives you a far wider field of vision than you'd get in a supermini.
Design and Build
This Tourneo Courier delivers honest van-derived design with refreshingly frank simplicity. The main visual change in recent times has been this revised front grille. Otherwise, the main thing of note here is just how much cabin space Ford has been able to fit into a car with a supermini-sized roadway footprint.
This may be Ford's smallest MPV but you wouldn't think that from a seat inside. The perception of airiness is helped by the vast amount of headroom - and by superb all-round vision with an expansive windscreen that stretches high above your field of vision. Everything falls to hand easily and the centre stack now looks much more up to date than it did when the Courier was first launched, with the option of the brand's latest 'SYNC 3' infotainment technology. In the rear, accessed via sliding doors, you'd be tempted to say that there's just as much room as you'd get in the far pricier Tourneo Connect model. That airy roof height certainly makes it feel like that.
Market and Model
The buying proposition here is pretty straightforward: one body shape, a single 'Zetec' level of trim and a single transmission choice, a 6-speed manual gearbox. It comes mated to a choice of engines though; either the 100PS 1.0-litre EcoBoost petrol unit I tried, which from launch was priced from just under £15,000. Or a 100PS 1.5-litre EcoBlue diesel, which at the time of this model's introduction was priced from just over £16,000.
Let's give you some Ford range perspective on that. The next model up in the brand's Tourneo People Mover range is the mid-sized Tourneo Connect, which comes only with diesel power. With the same 1.5-litre 100PS EcoBlue unit, an equivalent five-seat version of the 'Connect' would cost you nearly £6,000 more than this Courier model - which quite frankly, we think many family buyers would struggle to justify.
Cost of Ownership
One of the things that's completely changed with this design since its original launch as a van is its running cost efficiency. That's down to the installation of a pair of fresh powertrains that both now conform to the latest Euro 6.2 emissions standard. And the provision of a 6-speed manual gearbox in place of the previous 5-speeder. A little annoyingly, you have to pay a touch more to maximise the benefits of all of this engineering effort because the brand has elected to make its engine Auto Start-Stop system an extra cost feature (it's £180 more) - which seems a bit mean. Try and negotiate it in with the price you agree with your dealer.
Anyway, let's get to the figures, which for fuel economy have been measured according to the latest stricter 'WLTP' ('World harmonised Light vehicle Test Procedure') ratings cycle. The emissions stats we're going to quote here have been converted back to the older 'New European Driving Cycle' 'NEDC2' spec, since that's what a lot of rival models are still using. The 1.0 EcoBoost petrol unit I tried manages up to 43.5mpg on the combined cycle and 122g/km of CO2, or 41.5mpg and 131g/km of CO2 if you do without Start-Stop. What about the diesel? Well, for the 1.5 EcoBlue unit, you're looking at up to 52.3mpg on the combined cycle and 112g/km of CO2. Or up to 51.4mpg and 117g/km if you do without Start-Stop.
Ultimately though, what matters here is space and sensibility, both these things being predictably strong Tourneo Courier selling points. IAnd it obviously makes more sense than that conventional family hatchback you might have been looking at. But of course it's not as sophisticated or as stylish. Does that really matter? If you think not and you're one of the relatively few family buyers still looking for a compact MPV, then one of these ought to make your short list.
CAR: Ford Tourneo Courier
PRICES: £14,820-£16,130 - on the road
CO2 EMISSIONS: [1.0T with Start-Stop - WLTP] 122g/km [NEDC]
PERFORMANCE: [1.0T] 0-62mph 14.1s / Max Speed 107mph
FUEL CONSUMPTION: [1.0T with Start-Stop - WLTP] (combined) 43.5mpg
STANDARD SAFETY FEATURES: Twin front, side and curtain airbags / ABS / ESP
WILL IT FIT IN YOUR GARAGE?: Length/Width/Height mm 4157/1764/1741mm

subset: commoncrawl


text:
Chris Felix
Contributing Editor, Production Machining
Contributing Editor, Production Machining
Related Suppliers
Acquiring non-perishable tooling after a major machine purchase can require a large expenditure—one that is often uncomfortable for companies with limited budgets. In today's hyper-competitive marketplace (especially in the middle of a questionable economy), this cash outlay might even be considered crippling. A quick-change system from WTO Inc. is aimed at addressing these concerns for leaders focused on conserving costs and improving productivity.
Flexible Clamping
Featured Content
The QuickFlex quick-change system for driven toolholders is designed to save money in out-of-pocket tooling costs while reducing tool change time and providing greater flexibility. "Providing an ER collet chuck and quick-change system in one toolholder allows you to buy many fewer tools than you would have to otherwise," says Anthony DeHart, director of sales and business development at WTO USA. "Best of all, this flexible system doesn't compromise rigidity, performance or accuracy, which is great news for high precision contract manufacturers."
Officially introduced in 2012, the system is now available for the North American market, offering a complete toolholder program for the most popular turning center models using bolt-on turrets.
Specifically, Mr. DeHart says, the base unit allows customers to clamp tools directly into the ER collet of the toolholder—no additional purchases necessary. If customers acquire additional types of tooling in the future, they can be accommodated by using the QuickFlex adapters, which are mounted directly into the base unit.
"The base unit comes in a straight (radial) or right angle (axial) configuration, which, combined with the range of adapters available, covers virtually any machining process requirement, all in a single system," Mr. DeHart explains. "This approach enables the company to incrementally invest in a range of options with minimal initial capital requirements. It also accommodates the multiple setups and frequent change-overs that are required for the short manufacturing runs in today's production environment."
System Benefits
The system covers a range of different tool clamping adapter types and sizes and contributes to longer toolholder life. The modular design means that customers do not need to buy a complete quick-change system right away, but instead can begin by simply clamping the cutting tools directly into the toolholder using a standard ER collet.
For all manufacturers, time is money. The longer it takes to change from one tool to another, the longer production is paused. These setup delays can seriously cut into productivity and limit profits. QuickFlex's cutting tools can be preset while the machine is operating, meaning that the setup time for tool change at the machine can be significantly reduced.
Designed for precision and performance, the system also provides quick tool change with its one-hand wrench, which is used to hold the QuickFlex spindle while the large collet nut is tightened with the spanner wrench. Adapters (which use the built-in thread nut) are tightened the same way.
The system is also designed for flexibility. While the toolholder can be used without a quick-change system, a quick-change function can be easily added. Adding quick-change adapters after the initial purchase can reduce tool change time even more dramatically. The complete quick starter kit includes three different adapters and a one-hand wrench set.
In the past, changing tools has been difficult, time consuming, and in some cases, risky. The QuickFlex system is designed to address these issues. "With QuickFlex, our goal was to develop a compact, simple and safe quick-change system for driven toolholders," says Karlheinz Jansen, technical director and member of management, WTO GmbH.


text: Mobile Mechanic King Lake In need of a mobile mechanic in King Lake that can get to your location and fix your car related problems? Halls Mobile Mechanics are licensed mechanics operating in Melbourne that provide quality mobile solution to all your mechanical needs. Don't believe us? take a look at some of the kind comments our previous clients have left us (testimonials)


text:
User Reviews & Ratings - acetylcysteine-mecobalamin-levomefolate calc oral
Read user comments about the side effects, benefits, and effectiveness of acetylcysteine-mecobalamin-levomefolate calc oral.
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Reviewer: [email protected], 75 or over Male on Treatment for less than 1 month (Patient)
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I had to have a CT and my kidneys were weak so I need this to flush out my kidneys. It was a three day process to clear out them out.
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text:
Viktoria Tan Women's Northern Lights with zip fastening
Reference: 1225LETA
Tan Women's Northern Light boot with soft sheepskin lining, zip fastening and an unique Northern Light sole. Warm and stylish boot for Autumn and Winter.
|Heel height:
|Boot height:
|Boot circumference:
Size and fitting guide
Shoes and Ankle Boots
Marta Jonsson, crafts her shoes and boots with a standard C fit for the feet. Currently we do not offer half sizes. If you are in between sizes, or one of your foot is slightly larger take a size up. Often it is possible to adjust a slightly larger fit with a good quality ½ or full leather insole. *Selected Marta Jonsson styles are available in a size 42.
Please visit out new cheap hermes outlet store online.
|Women's shoe size
|Standard C Fit (Circumference of the widest part of foot)
|21.5 – 23.0
|22.0 – 23.5
|22.5 – 24.0
|23.0 – 24.5
|23.5 – 25.0
|24.0 – 25.5
|24.5 – 26.0
Foot width – How to measure?
- Use a fabric tape measure graded in centimetres, place flat on the floor with cm side facing down.
- Place the widest part of your foot on top of the tape measure.
- Pull the tape measure around the widest part of your foot, measuring the circumference of your foot. Normally the widest part of your foot is the joint next to your big toe to the joint next to our little toe.
- Measure both feet in this way and note the measurements of both feet.
Use the larger measurement in cm, as a guide to which shoe size is most likely to be suitable for you by reading the table above, set out in Continental, UK and USA sizes.
Having established your size from the table above, please follow the guidelines below on how we recommend measuring calf width and leg height to ensure the best fit with our boots.
Boot height – How to measure?
For each calf, or full length boot we specify the length of the boot (excluding the heel) in the product description.
- Sit on a chair with your feet flat on the floor and knees at 90 degree angle.
- Use a fabric tape measure. Hold the start of the tape measure behind the heel of our foot and measure up the leg at the back of the leg.
- Going by the height measurement given for your chosen boot style and size, you'll be able to see where about the top line of the boot will sit on your leg.
Leg width / Calf measurements – How to measure?
For each calf or full length boot we specify the circumference of the top-line of the boot shaft.
- Use a fabric tape measure graded in centimetres.
- Stand with your feet flat on the floor. If wearing trousers, make sure to roll up or take a second measurement if you want to use boots over your trousers.
- Wrap the tape measure around the leg/calf where the topline of the boot will sit, ensure the tape is snug around your leg/calf and measure to the nearest full cm. Measure both legs/calves to be on the safe side.
Heel height – How to measure?
Heel height for shoes can be measured in different ways. The ways in which we measure the heel & platform heights are as shown on the diagram below.
Delivery & Returns
UK / Ireland delivery information
|Delivery service
|Orders must be placed by 2pm to receive delivery on the next working day.* Delivery Monday-Friday only.
|Delivery within 3-5 working days*. Delivery Monday-Friday only.
|Republic of Ireland
|Delivery within 3 working days* Delivery Monday-Friday only.
*Please note that we are closed on Monday 2nd January 2017.
* Please note that weekends and public holidays are not considered working days. Outlying areas such as the Highlands & Islands of Scotland, Isle of Man & Isle of Wight may take slightly longer.
When receiving a parcel, you will be asked to sign for it as proof of receipt. If you are not there, a card will be dropped through your door stating how to receive your parcel.
If you would like some help or have any questions about our delivery options, please contact the Marta Jonsson Customer Services team by calling us on +44 (0) 208 881 0310 or emailing email@example.com
International delivery information
|Delivery service
|Europe (EU and EEC)
|Delivery within 3-5 working days *
|Royal Mail
|Rest of World
|Delivery within 5-10 working days *
|Royal Mail
International delivery is charged on a flat rate basis, regardless of the weight of your order.
We will endeavour to deliver to any location outside the UK/Ireland via Royal Mail and our staff will be more than happy to assist you through this process if you need any help.
For countries outside the EU, sales tax, customs and import duties may be charged once the parcel reaches its destination country. These charges must be paid by the recipient of the parcel. You may want to contact your local customs office for information on if / which charges will apply.
Gift Vouchers Delivery Information
How the Process of Buying Vouchers Works:
-After your order on our website for one or more of our gift vouchers is placed an email containing your online gift voucher code will be sent to the email address provided;
-Please note it might take up to one working day for the online gift voucher to be processed and emailed.
Order Errors:
-If you've made an error on your order, please email our Customer Service on firstname.lastname@example.com and we will do our best to correct it.
Returns and refunds
We hope that you love and enjoy wearing your fabulous new Marta Jonsson purchase, however we guarantee to refund any item you are not completely happy with when you return it to us in a saleable condition within 14 days of receipt.
There are two simple ways to return an order:
- To return by post simply fill out the returns slip & return along with the items in their original condition & packaging within 14 days of receipt. We do not pay for return postage this will be at your own cost.
- Alternatively you can return your order to your nearest Marta Jonsson store*. Please ensure you bring the returns slip as proof of purchase. You will also require the card that was used to purchase the order online. We are unable to exchange items; you would need to return items for a refund and then re-submit a new order. *Unfortunately we are not able to accept online returns from martajonsson.com through our department store concessions.
If you are returning items these remain your responsibility until they reach us at the address below & have been checked. For your protection we recommend that you send any return using a delivery service that insures you for the value of the goods.
All returns must be sent to:
Marta Jonsson Returns Department
Terms and conditions for Gift Vouchers:
-For security reasons we advise that when purchasing a gift voucher fill in the intended recipient's name in the Delivery information requested;
-The voucher can be applied at the Checkout for a purchase in equal or superior value to the voucher value excluding delivery charges;
-Please note that all the returns purchased with gift vouchers will be refunded with a gift voucher with a matching value to the original. This does not affect your statutory rights.
-The voucher can only be used once and in full amount;
-The voucher is valid for a period of 6 months from the date of purchase.
-The gift voucher can be cancelled within 24 hours (Monday-Friday) if the voucher has not been redeemed;
-Gift Vouchers cannot be returned or refunded, except in accordance with your legal rights.


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WASHINGTON, July 14 (UPI) -- The U.S. Supreme Court, before going on recess last month, narrowed affirmative action in college admissions as much as it possibly could without killing it.
A case accepted for argument next term not only threatens big trouble for what remains of race-based preferential admissions, but for gender-based admissions policies as well.
Last month's case dealt with the University of Texas. Next term's case deals with the state of Michigan. Unless the justices save affirmative action, proponents in the Michigan case warn, the nation's best universities and graduate schools increasingly could become enclaves for the elite.
The Supreme Court has wrestled with the concept of affirmative action in college admissions for decades, weighing whether diversity is so compelling an interest that public colleges and universities can treat applicants differently because of the color of their skin.
In 1978's Regents of the University of California vs. Bakke, a Supreme Court majority found the admissions policy of the UC Davis Medical School unconstitutional when it set aside spaces for minorities, but a plurality recognized that diversity was a legitimate goal.
In 2003, the high court went both ways, striking down the University of Michigan's undergraduate admissions policy but upholding the admissions policy of the Law School, though both used race as a determining factor.
In Gratz vs. Bollinger, the justices ruled 6-3 the university's undergraduate admissions guidelines were unconstitutional. The guidelines used a number of factors to evaluate an undergraduate applicant, assigning a numerical value to each factor.
Those scoring above 100 were considered eligible to fill the limited number of slots. However, minorities automatically received a 20-point bonus.
The prevailing opinion written by the late Chief Justice William Rehnquist said: "Because the university's use of race in its current freshman admissions policy is not narrowly tailored to achieve [the school's] asserted interest in diversity, the policy violates the equal protection clause" of the 14th Amendment.
The other University of Michigan case, Grutter vs. Bollinger, was handed down the same day with Justice Sandra Day O'Connor joining four liberals to form the five-member majority for a different result.
In Grutter, the university's Law School chose applicants based on a number of factors, including race, but gave no numerical weight to race. Instead, the Law School tried to achieve a "critical mass" of students, black and Native American, who might otherwise not be included.
O'Connor said in her majority opinion, "The law school's narrowly tailored use of race in admissions decisions to further a compelling interest in obtaining the educational benefits that flow from a diverse student body is not prohibited by the equal protection clause" of the Constitution.
She said the law school's policy survived even strict scrutiny, the toughest of three levels of scrutiny used by the courts (the lower levels are "reasonable review" and "intermediate review").
But, she warned 10 years ago, racial preferences should not last forever.
"It has been 25 years since Justice [Lewis] Powell first approved the use of race to further an interest in student body diversity in the context of public higher education" in 1978's Bakke, O'Connor said. "Since that time, the number of minority applicants with high grades and test scores has indeed increased. ... We expect that 25 years from now, the use of racial preferences will no longer be necessary to further the interest approved today."
Last month, the justices ruled 7-1 to narrow the use of affirmative action by state schools but fell short of striking down such policies altogether.
Justice Elena Kagan, who was U.S. solicitor general when the Texas dispute was in the lower courts, took no part in the case. Justice Anthony Kennedy wrote the majority opinion.
More than three-fourths of freshmen enrolled at the University of Texas at Austin under a state law that gives automatic admission to students in the top 10 percent of their high school classes. For the rest, the school considers a number of factors, including race.
Two white students denied UT admission under the policy challenged it in federal court.
A three-judge appellate panel upheld the admissions policy, and the full 5th U.S. Circuit Court of Appeals, one of the most conservative in the country, refused to rehear the case by a vote of 9-7.
The appeals court majority said UT's admissions program was "narrowly tailored," as required by the 2003 Supreme Court precedent in Grutter vs. Bollinger.
But the Supreme Court threw out the appellate ruling in the Texas case, saying it didn't conform to Grutter.
In effect, the majority opinion ruled, consideration of race had to be the last resort when trying to achieve diversity. Kennedy said: "The reviewing court must ultimately be satisfied that no workable race-neutral alternatives would produce the educational benefits of diversity."
Justice Ruth Bader Ginsburg was the sole dissenter, noting: "The court rightly declines to cast off the equal protection framework settled in Grutter. Yet it stops short of reaching the conclusion that framework warrants. Instead, the [Supreme] Court vacates the court of appeals' judgment and remands [sends it back] ... to 'assess whether the university has offered sufficient evidence [to] prove that its admissions program is narrowly tailored to obtain the educational benefits of diversity.'
"As I see it," Ginsburg added, "the court of appeals has already completed that inquiry, and its judgment trained on this court's [precedents] merits our approbation."
The new affirmative action case out of Michigan, accepted for argument next term, presents a much broader canvas for the Supreme Court's conservatives to paint on. Liberal Kagan again is not participating.
In the November 2006 election, 58 percent of Michigan's voters adopted Proposal 2, which amended Michigan's Constitution to prohibit discrimination -- or preferential treatment -- in public education, government contracting and public employment based on race, sex, ethnicity or national origin.
In other words, the state cannot discriminate against someone because of race or gender, but it also cannot give preferential treatment to someone based on race or gender.
Almost immediately following the election, a group of plaintiffs led by the Coalition to Defend Affirmative Action filed suit challenging the constitutionality of the amendment.
Under challenge, the full 6th U.S. Circuit Court of Appeals, based in Cincinnati, by a vote of 8-7 struck down the state amendment only as it applies to public schools, saying it violates the equal protection guarantee of the U.S. Constitution. It left the rest of the amendment intact.
"It is exceedingly odd to say that a statute which bars a state from 'discriminat[ing] ... on the basis of race' violates the equal protection clause because it discriminates on the basis of race and sex," the state told the U.S. Supreme Court in a petition. "Yet that is precisely what the [court of appeals] majority held here, in conflict with the 9th Circuit's decision" in another case, and the California Supreme Court in a third case.
"Michigan recognizes that affirmative action has long been controversial; some state entities use it for some programs, some do not," the petition said. "But until now, no court has ever held that, apart from remedying specific past discrimination, a government must engage in affirmative action. This [Supreme] Court has said just the opposite, holding that all racial classification by government entities are presumptively invalid and subject to the strictest scrutiny. ...
"In the face of that exacting standard, the 6th Circuit [appeals court] held that [the ban on college admission affirmative action] violates the equal protection clause by denying minorities a 'fair political process.'
"In reaching that conclusion, the court of appeals did not say that the process through which Michigan voters adopted the measure was unfair," the petition said. "Rather, what is 'unfair' [according to the en banc majority] is that supporters of affirmative action can no longer obtain affirmative-action programs on a university-by-university basis. That conclusion cannot possibly be right."
The petition pointed to O'Connor's opinion in 2003's Grutter vs. Bollinger that suggested "a 25-year window allowing race-conscious admissions programs in higher education, and it invited states to experiment with race-neutral alternatives for achieving classroom diversity. Eight states have accepted that invitation: Arizona, California, Florida, Michigan, Nebraska, New Hampshire, Oklahoma and Washington. But more than 2 million Michigan voters have now been disenfranchised of their choice to eliminate considerations of race in education by a one-vote margin en banc decision that misapplies this [Supreme] Court's equal-protection precedents in several ways. Michigan respectfully requests that the [Supreme] Court ... consider whether a state's decision to require equal treatment in higher-education admissions violates equal protection."
The challenger of the affirmative action ban, Coalition to Defend Affirmative Action, sees the case in a quite different light.
"Until the passage of Proposal 2, the elected university governing boards had complete control over all admission criteria, and the state's residents could therefore add to, change, or delete any of those factors through a simple majority vote by the faculties or by the elected governing boards, who supervised those faculties," the coalition told the U.S. Supreme Court in its own brief.
"Proposal 2, like Proposition 209 before it" -- California voters enacted their own ban in 1996 and the federal and state courts have upheld it -- "selectively changed that. The universities may now adopt any factors authorizing departures from their baseline criteria of grades and test scores for any purpose -- except that they may not consider race for the purpose of admitting black, Latina/o or Native American applicants."
The Michigan parents of minority applicants "may no longer even propose that the governing boards adopt the exact plan that this [U.S. Supreme] Court held was the only practical means by which their children could be admitted to the state's leading universities" -- a plan outlined in 2003's Grutter vs. Bollinger.
The appeals court right held that the ban violated the equal protection guarantee of the U.S. Constitution, the coalition brief said.
The brief argued, "The proponents [of Proposal 2] claim that its ban is neutral, but the only explicit consideration of race is for the purpose of admitting minority students. In practice, Proposal 2 hands the opponents of minority admissions a legal sword [a private right to file suit] to wield whenever and wherever a university admits what the opponents believe are too many minority students."
The ban has practical effects in "the real world," the brief said.
State Attorney General Bill Schuette, who asked the justices to reverse the appeals court, "claims that it is impossible to determine who Proposal 2 actually burdens. But in the real world, there is no doubt on that question. In 2003, the University of Michigan's attorneys told this [Supreme] Court that eliminating affirmative action would cause a one-third fall in minority admissions at its Law School. They were too optimistic. In six years, Proposal 2 has slashed the share of black, Latina/o and Native American students in the entering classes in Michigan's undergraduate college by one-third, slashed the share of those students at the Law School by 40 to 50 percent and slashed the share of those students at the Dental and Medical Schools by 70 percent or more.
"The president and chancellors of the University of California have informed this court that the effects [of Prop 209] in California are even worse," the coalition brief said.
"The number of black students in the entering classes at UCLA and Berkeley has fallen by 50 percent while Latina/o admissions have not reached pre-209 levels despite a 25 percent increase in the percentage of Latina/os in that state's high-school graduating classes. As the UC officials informed this court, they have found no way to reverse that precipitous fall."


text:
COMMERCE CITY, Colo. — Six months ago, Colorado Rapids midfielder Shane O'Neill was a high school senior, ready to head to the University of Virginia on a soccer scholarship.
But in what's been a whirlwind 2012, the 19-year-old Homegrown player is now a rising star for the Colorado Rapids, and now, freshly returned from making his international debut at the Under-20 level for the US national team.
O'Neill (above, left) made his U-20 debut at the Marbella Cup in Spain earlier this month, playing 65 minutes in a 2-1 friendly defeat to Canada. An eye injury prevented him from playing in the final two games of the tournament, but in the meantime, the Ireland-born, Colorado-raised youngster still managed to receive valuable experience at the international stage.
"I got confidence to see that I can play at that level," O'Neill told MLSsoccer.com. "Overall, it was a really good trip for me."
The holding midfielder only signed his first professional contract in June, but right away the Boulder, Colo., native found himself competing for a spot on the field. In July, O'Neill debuted for the Rapids in a 2-1 friendly win over English Premier League side Swansea City, and in September, he made his first MLS appearance in a 3-0 win over Portland. And on Oct. 10, O'Neill started the Marbella Cup opener for the US, the icing on the cake in what's been a big year for the youngster.
"It has been a good year for him," Rapids head coach Oscar Pareja said. "[He's] experienced a year with the professional team, was called to the national camp, made his debut, and hopefully we can see some action from him [in the Rapids' season finale against Houston on Saturday]."
The lone potential holdup for O'Neill is an eye injury that he suffered in southern Spain which kept him out of the final two games of the tournament.
"I want to be 100 percent, to make sure there's no lingering problems," O'Neill said. "We've got a U-20 camp in December. It sounded pretty good [that I'd get an invitation to attend]. Hopefully, I can just stay in that through qualifying and get back to 100 percent."
Chris Bianchi covers the Colorado Rapids for MLSsoccer.com.


text:
Due to the recent problems with the forum, we are moving the forum to a new server. We're taking the opportunity to move the rest of the 808state site to the same server.
Posting will be disabled as of 10pm tonight. Also the URL of the forum will change. It will be in a more logical location (well, for me at least) and I hope it will be the last time the URL changes.
Can't say how long the outage will be for, but expect up to 24 hours...
Sorry about this, the timing is not perfect, but I'll be a lot happier once this has been accomplished.
Forum and site maintenance as of 10pm UK time tonight!
Discuss non-musical topics that are not related to 808 State or music.
Moderators: Pob, markus, nickking, Ancodia
Post Reply
3 posts • Page 1 of 1
Forum and site maintenance as of 10pm UK time tonight!
Last edited by markus on 14 Dec 2002 23:00, edited 1 time in total.
Post Reply
3 posts • Page 1 of 1


text:
I have been inspired by Chen to talk about bash…
I have been using ksh for many years, and I mean ksh88 not ksh93. The main reason is, I want my script to run the same way in any Unix flavor.
ksh93 has never been too much popular. I used it a few time to sleep half a second
echo sleep 0.5| /usr/dt/bin/dtksh
ksh has a lot of nice features. I just used one of them in my script :
$ typeset -u name
$ read name?"Enter your name : "
Enter your name : Laurent
$ echo $name
Way easier to force a variable to be uppercase rather than using echo|tr etc
Bash has some nice features too, but unfortunately every OS release come with a different bash version, which is the same pain as perl when you want to write a script that last for a decade or two.
Ok, just4fun
$ mkdir -p {a..z}/{1..9}
... create directories a/1 a/2 ... z/8 z /9
$ [[ text =~ t..t ]]
... check if text matches regular expression t..t
$ echo ${text/pattern/string}
... replace pattern by string
The first two commands require bash3, the last is just fine with bash2.
Have fun shell-scripting 🙂


text:
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text:
Professor of Classics and Ecclesiastical/Patristic Greek Language and Literature
Evie Holmberg is a professor of Classics and Early Christian Literature. She is also an Art Conservator/Restorer. Her latest work concentrates on symbolic representations in myth as they relate to ancient spiritual paths and experiences produced through prayer, meditation and recent controlled experiments in psychoanalysis. She has also done extensive work in Art Conservation/Restoration and its relation to the social and cultural environments that influence the reconstruction and exhibition of ancient art.
Evie Holmberg joined the faculty of Hellenic College Holy Cross in 1979, and she has held a joint appointment in both schools as a professor of Classics and Ecclesiastical Greek since 1993. Since 2013, she has been professor of Classics & Ecclesiastical Greek Language and Literature at Holy Cross. Since 1977, she has also worked as director of research projects and art conservator at the Fog Art Museum Harvard University, L.A. County Museum, and the Museum of Fine Arts Boston. Because of the breadth and diversity of her background, she has adopted an interdisciplinary and diachronic approach in her scholarship and teaching. Her work and publications include sample analysis of works of art for the determination of their dating, provenance and history of restoration, translations and commentary of Greek texts of Classical, Hellenistic, Byzantine, and Modern Greek origin, as well as diachronic and comparative historical studies.


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Author Brian Azzarello's Wonder Woman has been one of our favorite books of the DC Comics relaunch, what with its profoundly creepy take on Greek mythology and the Olympic pantheon's political machinations.
And in the latest issue of Wonder Woman, the heroine is caught between the blubbery, tentacled Poseidon and the candle-headed death god Hades. Courtesy of DC Comics, here's an exclusive five-page preview of the weirdness.
This issue, artist Tony Akins gamely fills in for Cliff Chiang, who you may remember drew the Japanese Justice League. I really enjoy Akins' Cerberus — a three-headed hellhound isn't something I'd normally describe as adorable. Wonder Woman #6 comes out next Wednesday, February 15. Here's the plot synopsis:
Wonder Woman #6
Written by Brian Azzarello
Art by Tony Akins
Covers by Cliff Chiang
Hades and Poseidon both have designs on the kingdom their brother Zeus left behind, but Wonder Woman doesn't intend to let their turf war decimate the realm of man! It'll take a big lie and some help from the mystery man known as Lennox to stop a holy war from breaking out – but what does Lennox know that Wonder Woman doesn't?


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Priority: Mars
In the conversation before Priority: Mars commences, you can stop James mid-speech while he argues with Shepard on the Normandy for bonus Paragon or Renegade points. Just wait for the blue icon to appear on the left or the red icon on the right and hit the button shown (LEFT TRIGGER or RIGHT TRIGGER usually).
You won't have much time to reunite with Joker and EDI as you'll soon be on a shuttle to Mars with Kaiden/Ashley and James Vega. You can award 2 Power Points to your Squad Members as soon as you touch down. You'll also be able to award 5 to yourself. Definitely add Concussive Shot to James's repertoire and, in general, add new Powers so you have a bigger arsenal at your disposal. Save the upgrading for later.
- See the Powers section for complete upgrade trees
Mission Enemies
Follow the waypoints towards the facility. Examine the corpse after you jump down by clicking the RIGHT STICK. Do this again to examine the armored enemies in the distance. These are Assault Troopers. They are not shielded. You will now have a Sniper Rifle, the M-92 Mantis I, to use on the distant troops.
Use a grenade power if you or a Squad Member has one. Inferno Grenade, Sticky Grenade and the like will catch the enemies of guard. Snipe them from your high position.
Stay to the left after you pass the initial group and, by the Mako vehicles, take cover behind a short wall and secure the entrance to the facility. Remember to direct your Squad Members to use their rechargeable attacks.
Once inside, hit the elevator panel.
Prothean Archives
After the long cutscene with Liara T'Soni, it will become clear that Cerberus is the enemy on Mars. Your goal is to find the Prothean Archives before Cerberus does.
Immediately head to your Squad menu and upgrade Liara's Powers. Add Warp and another ability. You'll want to use Singularity on the enemies above the area.
This will lift the Assault Troopers skyward and allow you to take potshots at them. Use this technique to clear the room.
Now, look for the vehicle lift controls in one corner. Activate these and you can use the listed yellow vehicle to bypass the broken elevator. Climb up the stepped ledges beginning at the top of the ramp (and grab the ammo as well). You can sprint across the vehicle you raised and get to the upper level. Head through the green panel door into the next area.
In this room there are controls for the pedway. You can also loot the area for the following items:
- Datapad: Read this pad on the benches for XP.
- Ariake Technnologies Gauntlets - Pick this armor piece up in the small office above some ammo. You can change armor later on the Normandy in your quarters, but any piece you pick up now will be automatically equipped.
- M-4 Shuriken I - This Submachine Gun can be found in the office on a downed trooper. You can equip weapons found in the field immediately, but you can only equip one type of each weapon at a time. You cannot modify weapons in the field. You can change weapons on the Normandy and at certain locations during missions.
- Medkit - There is a Medkit in the office as well.
Activate the Security Console by Liara when you can. This will open the door in the area and introduce you to Dr. Eva. Head out the green panel door on the upper platform and out the airlock.
Climb down the ladder outside and run down the long path towards the ladder.
- Kassa Fabrication Chestplate - Pick up this piece of armor at the bottom of the ladder.
Find your way across the ramps to the second airlock. In the darkened laboratory your flashlight will automatically turn on as you step into the shadows.
- Datapad - XP. This is right in your path.
- SMG Scope I - This Weapon Mod can be found by taking the central stairs to the bottom of the darkened lab and hooking around to the right. It's on a counter. You can upgrade your weapons at the bench in the next area.
On the other side of the glass windows are two enemies. Use Liara's Singularity ability to float them both in the air. This should also shatter the glass. Now finish them off quickly.
Explore the small office to find the Environmental Controls. Remember to assign Power Points to Squad Members if you level up!
- Medical Station - A Medical Station is on the wall by the Environmental Controls in the small office. Use this to recharge your med supplies and get some XP.
After activating the Environmental Controls a cutscene will allow you to get some Paragon/Renegade Points while interacting with Liara. Enter the green panel door in the now-pressurized room. On the other side you'll hear some enemies ahead. Use the bench to the right of the door you entered to upgrade your weapons before moving on.
- SMG Ultralight Materials - Snag this Weapon Mod off of a dead body by some crates before heading up the stairs.
The Guardians you encounter in the next hallway have shields that simply cannot be penetrated. Your best option for now is to use Liara's Singularity to lift them helplessly off the ground. Shoot them as they flail. Alternately, you can snipe a part of the their exposed body OR snipe their heads through a slot in the shield itself!
The long hallway is filled with Assault Troopers, a few shielded Guardians and a Centurian at the far end. The latter enemy is the only new type, and it has shields. You can fry the shields with any sort of fire-based weapon, like Inferno Grenade, Incenerate or an attack like Overload. You can probably just shoot these early enemies a lot to get thorugh their shields.
The adjacent lab at the end of the hallway has a contamination routine sweeping it. Two control panels allow you to stop and start this. You want to stop it at a wide angle so it exposes the Weapon Mod on the right side of the room, facing it. Patiently wait and hit the panel when the sweeping barrier exposes the item.
In the contaminated lab you can pick up some loot.
- Shotgun High Calibur Barrel - This is in the center of the room.
- Datapad - XP. On a table in the center of the contaminated lab.
- Sniper Rifle Extended Barrel - Do not miss this awesome Weapon Mod! This must be accessed by pausing the sweeping decontamination field at the right position.
- Medkit - There is a Medkit in the center of the room.
In the next hallway you can find your first Shotgun on a downed enemy.
- M-23 Katana I - Pick this up on a corpse in the hallway just before the tram.
The Auto-turret
This miniboss of sorts cannot be taken out, only avoided. The game's tutorials will show you how to go from one point of cover to the next. It's important to learn these skills, including rolling from one cover point to an adjacent on (hold LEFT or RIGHT on a stick and hit ACTION) and moving around corners under cover (click the LEFT stick).
Once you get around to the side of the turret it will go offline. You can now enter the green panel door. The turret control room is a good place to use your new Shotgun because of its tight quarters. Grenades work well too, just be ready for a Centurian with shielded armor. Loot the room once it is clear.
- Sniper Rifle Concentration Module - This ugrade is on a rack by the turret controls.
- Datapad - XP. This is by the turret controls.
Hit the Auto-turret controls and a long cutscene will play. Cerberus is making Husks apparently. Tell Kaiden/Ashley to trust you and get some Paragon/Renegade points out of it. After this Shepard will pull a Han Solo and you'll be able to access a tram.
In the next room you can tell your Squad Members to move to locations to flank the incoming Cerberus enemies. Tell them to go to locations on each side of the door for some XP. To do this on a controller, hit the D-pad LEFT and RIGHT to command each Squad Member to go to a separate location.
You should stay on the upper level. A good spot is ABOVE the door, but there is also an ammo supply on one side of the upper area so this is a good spot as well. The only enemy that will give you trouble is a Centurian. Remember to fry the shields with an anti-shield Power or ammo (fire, Disrupt).
Two shield-bearing Guardians should bring up the rear of the enemies. Hit them with well-placed sniper shots (go for the slot in their shield for the Mail Slot Achievement / Trophy) or a Singularity. Now, get on the tram beyond the large gate where the enemies appeared and hit the Cablecar Control panel.
Get ready for enemies with a Shotgun equipped. Pepper them with some shots and a grenade, then dash across the gap to their car and use melee attacks to finish them off. Hit the next control to continue.
In this room you'll encounter many enemies, but nothing new. The cover spots in the depressions in the center of the room are great. Just make sure to take full advantage of your Squad Member Powers here. Don't leave the area without this loot!
- M-15 Vindicator I - This Assault Rifle can be found at the end of the hallway in a dark corner by the large door.
- Shotgun Shredder Mod - This upgrade is on the other side of the door.
- Medical Station - Use this station in the central office.
At this point it should be noted that when you choose your weapon loadout, the Weight factor in the middle of the loadout screen will show the loadout's effect on your Power Recharge Speed. Heavy weapons mean slower recharge times. You can opt of any weapon type to lighten the load and even INCREASE your Power Recharge Speed. Later you will be able to purchase and find Upgrades to improve your weapon weights.
The next room leads to a long cutscene with the Illusive Man. After this a chase scene occurs.
Chasing Eva
Sprint after Dr. Eva around the curved edge of the room. A counter in the bottom right corner of the screen will show your distance from her. If it turns red, you are in trouble. Stay close or you will be forced to restart.
In the next room, hit the green panel to enter the security office, then hit another panel to lower the glass and hop over to continue after Eva. Climb the ladder and cross the exterior area after Eva. Her shields recharge too fast to allow you to do any damage.
She will run down a ramp and head for a shuttle, initiating a cutscene. After this, Eva will run at you, shields down. Shoot her a half dozen times in the slow-motion event and she will be dead. Unfortunately, Ashley/Kaiden won't be much better off.


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My Pizza Oven: Leyway, Making Pizza in Paradise
Q&A about home pizza ovens.
I discovered today's MPO subject via the My Pie Monday feature when she submitted a photo of her Margherita pizza. She was kind enough to put herself in the hot seat for us. And, wow. Turns out she's from Cebu, Philippines. Talk about pizza in paradise. —The Mgmt.
Name: leyway
Location: Cebu, Philippines
Website: flickr.com/photos/[email protected]
Wait! Holy crap. You're from Cebu, Philippines?!? That's like a freakin' paradise. Can we all have your life? ... OK ... First question ... when did you put your oven in? Did you build it yourself or have someone build it?
My dad got it for me, he supervised the work, of course. He had two guys working on it. My dad is a contractor, so he knows his stuff.
Nice. I hope you make pizzas for him. ;) How often do you use it?
We do have a pizzeria, which I own, so it's used every day. I get my wood from a friend from college so it works out I guess. I used to make the pizza every day, every night by myself all the time. But as of the moment, it's run by a different management since I went to trade school to learn more about bread and yeast. I always strive to be the better version of myself, and I knew that a lot of the pizza masters, like Anthony Mangieri, were bakers first—so I always knew that I just had to leave it for all the right reasons.
Oh, wow. I didn't realize you were running a pizzeria out of that oven! Cool. I guess you're basically our first pro MPO interviewee. ... So, I'm wondering, then ... do you cook anything besides pizza in it?
No. I haven't tried, though. I wanna cook bread in it, but I don't usually have the luxury of time on my hands.
What style of pizza do you normally do?
I strive to make a good Neapolitan pie.
What's your favorite topping or topping combination to make?
When I first started making pizza, my favorite was a Margherita with sausage and bacon. It was awesome. Then as I kept learning about dough and yeast (before trade school), I liked a Margherita with plain sausage. Now it's just a plain Margherita. When you know how to rock a pizza and make it taste so good with just a few ingredients I guess that's when you know you're on the right track.
Do you cook for friends/neighbors?
Yeah, I always invited friends. I always wanted feedback and wanted to know what they had to say about it.
What does your family think of your pizza madness?
They already know I'm crazy. They have learned to accept that.
Where do you go for pizza in your area (when you're not making your own)?
Where I come from there's not a lot of good pizza. So I usually make it by myself or Pizza Hut. But I try not to go to Pizza Hut as much as possible. Haha....
I probably don't even have to ask, but it's now standard ... what's most important to you: crust, sauce, or cheese?
Crust fo sho! I think its a really difficult thing to master, and the thing about it is that you never really get it right all the time, since there's so many variables you cannot control. Making a great dough/crust to me is like making great wine. Its such a fine art that takes alot of time and love to master.
What one thing should NEVER go on a pizza?
Oreo. Snickers. Anything that should be on thisiswhyyourefat.com should NEVER, EVER be on a pizza.. EVER.
Weirdest pizza you've ever eaten?
I dont know. I don't think they were weird. I always ordered a Margherita or anything that didn't have the kitchen sink for a topping.
What's the farthest you've traveled for pizza?
I don't know about farthest, but before I opened a pizzeria, I went and ate at every pizzeria this city has to offer. My conclusion is that... it's NOT GOOD.
LOL. Isn't it in your best interest to say that? ;) ... OK, last ... anything you'd like to get off your chest?
I really hope this country gets better pizzerias. Not a lot of good choices here. It's 2010. It's about time! Well, I guess, if anyone needs help with anything with dough or questions about pizza, I'll try my best to help anyone with absolutely anything. If you're in the same city as I live in, hit me up and I'll make you a pie with love.
Thanks for playing, leyway!
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Perhaps if you've been to The Merchant Company or visited any other of the holiday sales in the area you've seen these adorable, fantastic and totally covetable illustrations from Bluebirdie Bootique, by artist Christina Siravo. Feast up on some eye candy and start making your gift list for Sunday, Dec. 2nd at Mayo Street Arts! Click on the images for links!
We'll see you this Sunday at Mayo Street Arts, 10 Mayo Street in Portland from 10am to 4pm! 🙂


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Late local historian honored
July 23, 2009
Freedom New Mexico
The New Mexico Historic Women Marker Initiative is set to honor Rose Powers White, historian of the Portales area's early days of settlement, with a historic roadside marker.
A dedication and reception is scheduled for 4 p.m. July 30 at the Portales Public Library. State Sen. Stuart Ingle, R-Portales, will speak.
Ruth White Burns of Clovis, White's daughter, said when her mother moved to the area in 1923, there was no written local history.
White began collecting and recording the experiences of her husband's family, who came in 1882, and of other "old-timers," Burns said.
The initiative aims to recognize historically significant women with roadside markers in each county and pueblo, and on Apache and Navajo lands, according to a news release from the organization.


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The annual Monster Buck Classic We Are Kansas deer hunting extravaganza was a great show and yes there were plenty of Kansas monster bucks.
Monster Bucks
The doors opened Friday afternoon at the ExpoCentre in Topeka on January 26, 2014 to a good crowd of avid deer hunters and vendors and it was a fun filled weekend. With the name Monster Buck Classic the deer hunting show lived up to it's name and there were plenty of big Kansas brutes to be seen.
The Monster buck contest had some awesome entries and there was a new King of Kansas non-typical crowned as Lucas Cochren's 238 4/8″ King of Kansas Non-Typical fell to the a non-typical buck taken by Cade Hays with a net score of 239 7/8″, a small 1 and 1/8 inches difference! Both are awesome bucks.
There was so many great venders this year with some really cool hunting products. I saw so many good deer hunting products and will definitely be getting a few of them to get ready for next season. One of my favorite products was the INFERNOEPS™ element protection system. It is a cold weather suit that easily makes into a backpack and I tell you I was impressed with all the features. Hopefully I will be able to do a product review on this bad boy, very nice. If you get a chance go by and check out INFERNOTEK.
There were many great seminars and and the headliners were Mike Hunsucker and the Heartland Bowhunter tv show cast, Matt and Jessie Duff co-hosts the popular Friends of NRA television show on the Outdoor Channel, Grant Woods wildlife biologist, Miss Kansas Theresa Vail, Dan Thurston of Drury's Bow Madness, Torry Cook world champion predator caller, Steven Fuller host of "The Huntin Grounds", Zac Cooper Little man big dreams, Marian Kincaid of the television reality series "Mudcats".
It was nice to get to know some of them a little and talk deer hunting. And one of my favorite events was the celebrity bow shoot. Dan Thurston, Matt Duff, Mike Hunsucker and the Heartland Bowhunter crew all did some great shooting with there bows. Matt Duff did great even though he borrowed someone else's bow to shoot.
We had a great time at the Monster buck Classic this year and look forward to another great show next year. I'm already getting ready for next deer season and plan on doing all I can to get a big Kansas brute with my bow on film and hopefully he'll be big enough to take one of the King of Kansas crowns. I might as well dream big!


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Jack Russell Originals
From The Tower of London to The Bradman Museum in Australia Jack Russell original oil paintings and pencil sketches are in public and private collections worldwide. Each piece of Jack's work is unique. In fact in the art world Jack himself is unique. The former England Wicket Keeper has now been a Professional Artist for nearly 30 years and enjoys painting a variety of subjects.
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Praga Racing is the latest division of the Praga Manufacturing company, with a somewhat familiar past (to European automakers) of building cars, then motorcycles, then trucks, then buses, then tanks, then airplanes, and now race cars.
But wait, what series does batmobile-lookin' thing race in? Well it's kind of a funny tale; Praga teamed up with Radical to create a new series called the Supercar Challenge Superlights, to race in support of the regular Supercar Challenge series. Praga planned to enter 10 of their R1s into this newly minted series, but due to workers striking at the Spanish wheel suppliers' factory, they could only procure enough wheels to enter 3 R1s in the debut race. Slovakian racing at it's best (worst?).
A little more about that car: (which I can talk about since reading Roger Garbow's spinney story for Road & Track) It's got a Renault naturally aspirated 4 cylinder making about 210hp, capable of pushing the miniscule LMP1 look-alike all the way to 165 mph. It weighs in at a paltry 1300 lbs, and is capable of a whopping 1900 lbs of downforce. That's like, Men In Black-upside-down-driving in a tunnel capable downforce. Impressive.
Monticello Motor Club is launching a new racing school, featuring the first 3 Praga R1s in the country. A weekend with instruction will run you upward of $5,000, once again reinforcing something we already know; racing ain't cheap. Last night they brought chassis no. 3 down to the Classic Car Club Manhattan to feature for a special happy hour event. No one believed it was from Slovakia, not sure why.
Here's a quick video of the Praga unloading. The thing is so low and so carbon fiber, it took a while to jimmy it back and forth to finally get it inside CCC. Well worth it:
Check out the full gallery below:
Keep up with CCC on YouTube, Twitter, and Instagram (@cccmanhattan)


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|Biosequences .. Software .. Molbio soft .. Network News .. FTP
Given the fact that we routinely pump out anywhere from 40,000 to 60,000 e-mail messages per day, the mail queue on net.bio.net is usually rather large. Unfortunately in the last two weeks a problem appears to have developed which has enlarged it even further. Those of you who follow Internet security issues have probably heard that the UNIX mail program called "sendmail" is a frequent target of hackers who use holes in it to try to break into computer systems. Thus software upgrades are needed to plug security holes as they are discovered, and we try to stay on top of these necessary changes here. Unfortunately the last change may have backfired. We are investigating the hypothesis that a recent upgrade to a new version of sendmail at net.bio.net about two weeks back may have aggravated mail distribution problems from here, leading to an enlarged mail queue. We are taking steps to correct this. Messages posted via either e-mail to net.bio.net or via news would have been distributed as usual via the news system but many messages have stalled in the mail queue for other reasons. Thus e-mail users would not have seen all of the messages that news users have read to date. Dave Mack here is taking steps to "flush" the queue and get these messages delivered as soon as possible. These steps may result in some people getting (1) copies of older messages that have been stuck in the queue for a few weeks and (2) duplicates of some messages. Our apologies for the inconvenience. We are trying to get things back to normal ASAP. Sincerely, Dave Kristofferson BIOSCI/bionet Manager biosci-help at net.bio.net