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This is for my friend, Josh Gilman, a talented and generous person who is impossible to forget. He could change the life of another during a brief interaction, maybe because he didn't see any interaction as "passing," and appeared (and really did, I believe) to give all of himself to a person or a situation regardless of how small or insignificant it may be. This is what many people remember him as: someone who could be discussing the most personal and profound things with a stranger within minutes of meeting, someone who was as thrilled about life and its possibilities as we should all be, and maybe once were.
Perhaps more than anyone else I know, Josh made his life be about beauty and truth. What generations of people romanticized and further generation maligned and made fun of as cliché, he pursued in earnest and, I would say, with success. When he lived in Colorado, Josh would sometimes face his amp towards the Sangre de Christo mountains and play guitar to the uninhabited distance. If this sounds silly, the fault is with my writing. Or maybe with our stupid jaded times, because, I assure you, we may be endlessly rediscovering things others discovered previously, but this is just what being human is about. No two loves are ever alike, as no two sunsets are ever alike.
Josh spent much of his life traveling, abroad and in the U.S., for pleasure and in pursuit of ideas, people, or beauty. He'd hiked the Appalachian trail, where a bear raided his food and left him to walk a two or three day stretch of the way hungry. To my knowledge, he camped in Yosemite, visited the Upper Peninsula of Michigan, lived in the San Luis Valley in the high Rockies. I have beautiful pictures he took in Mexico, as well as from multiple trips in Southeast Asia, where he biked the length of the Malaysian peninsula to Singapore and eventually to Sumatra to see the Orangutans before they are eradicated from the wild. He spent significant amounts of time in Thailand on multiple trips and wanted to settle in Chiang Mai for good, though on his last trip there he came upon a politically volatile and unstable situation which thwarted any plans for staying. Josh also travelled to meet writers and poets he liked, or in homage of ones already gone. Josh admired Gary Snider, the beats in general, Thomas Merton, Thich Nhat Hanh, Jim Harrison, Patti Smith, Neil Young. He travelled to meet Doug Peacock in Montana, and to hear Amiri Baraka speak in Madison, as well as others, I'm sure.
I don't remember meeting Josh when we went to grade school together, but sometime around then I came over for lunch. We weren't close friends and I didn't know him that well, and hanging out on this occasion was the result of living a block apart and sharing the walk to school on occasion. I don't think we were even in the same grade, since they put me in a class with younger kids because I had just come over to the U.S. from the U.S.S.R. and didn't speak good English yet. I remember Josh striking me as an easy person to be around, and generous, more like the Russian kids I knew in that regard than American boys. I think even then, he saw material objects as meant to be shared and used for the purpose of making others happy. When we became friends years later, this was among the qualities that impressed me most about him. Without any pretense, like it was the most natural thing in the world, Josh did things for people he cared about, things to make them feel good.
I would get to know that house really well some years later, housesitting when Josh was living in Colorado. He was jealous that I got to hang out with Juniper, the brilliant border collie. Much of the handyman work the place has seen over the past decade has been my doing, for better or for worse. A couple years back, I spent a beautiful summer afternoon making a watercolor of the facade from across the street, a present Josh wanted made for Renee, his mom. Later in the day, a neighbor lady came to Renee to ask her if she was aware a man was drawing the house. In the heady days of Bush-era paranoia, perhaps she thought I was scoping out the place as a terrorism target.
In the mid or late 2000s I spent the summer living in the garage, which Josh transformed into a remarkably homey space with Asian hangings, candles, furniture, and whatnot– among the latter, a woven prayer rug from Afghanistan with an AK prominently and intricately depicted in the center, and a theme of weapons continued in the margins. Not sure where he got that thing. He had a way of creating sacred or liminal spaces which really worked in a magical, unfathomable way, half ritual and half empathy. We cooked food on a coleman stove and drove Renee mad burning huge bonfires and playing music into the night, as friends came and went with the ease afforded by a garage hangout and summer nights. The culmination of that period was the art rummage sale we held early in the fall, at which I sold every single piece of art I ever made up to that point to a generous friend and gave away many drawings to others. It was billed as "Full Moon Gallery," a benefit for the Chiang Mai Artist Collective (which never materialized but was intended to be the next phase of our lives– more clearly so in Josh's mind than mine).
The artist collective in Chiang Mai was for us, but it was also meant to be a place and an experience available to anyone who wanted to escape the mindfuck that is this nightmare of a creatively stunted and competitive society for a simpler and cheaper alternative on the other side of the world, as well as for friends he had made there on previous trips. It would be a place where people could live in beauty and make art to send back to the states to sell. Almost as soon as he got back to Thailand, I think, it was clear that things had changed and the plans had become an impossibility: the friends he looked forward to seeing where in the dumps, the country was on the brink of rioting, the prospect of settling down was all but impossible. Biking the length of the Malaysian peninsula on the way toward Sumatra, hoping to see the last of the remaining wild Orangs before they were wiped out, he encountered angry and fearful people along the way. Later in the trip, armed with razorblades and a bottle of rubbing alcohol, he tried to get rid of the large "Siempre" we had tattooed on his thigh that summer before he left. Alone in some hotel room in some giant city, it must have been quite the opposite of what he hoped for when he left for Thailand with every intention of staying. I can't fully wrap my head around this, but I can't wrap my head around the way he just decided he was gonna start an artists' collective across the world and went for it, with the assumption that if he built it, people would come. This is how legends are made. I don't think I ever had this kind of confidence and certainty in my vision or myself.
Josh was genuinely happy to see people he cared about succeed, and was unstintingly generous with his time and energy towards this end. The art rummage was one example of his faith in me, commissioning the painting of their house another. At the same time, he could be utterly mute about his own art and accomplishments. I never learned about the book of poems he had collaborated on with Antler and two other poets, "Four Against the War," until I googled his name this year. I don't think we were friends when he was writing most of those poems, and he never showed them to me, so I was only to realize what a talent he had when I couldn't tell him so anymore. This is the price of exceeding humbleness. Its not that I was ever unaware of how special he was when I did have the benefit of his company, but we don't make a practice of telling as much to one another, assuming that the unspoken fact is confirmed automatically by virtue of our bestowal of our friendship on another. Of course this may or may not be the case, and probably isn't the case when you are depressed or agitated and your entire demeanor sends the message that the whole universe is shit.
I saw the gnarly scar on Josh's thigh where the "S" used to be when he came back later that winter, but even though I lived in a rented flat just up the block from him for the rest of that year, we spent little time with each other compared to the summer previous. At some point during the following year Josh had cloistered himself off from me and everyone else I knew for the better part of a decade. Because I didn't see him for so long, I can't be sure when the change in him took hold, and whether it did all at once or gradually over those years. It was clear that he returned from Asia shellshocked, but not as clear what happened and what it meant. Maybe he was going through the protracted funk of trying to figure out how to live meaningfully in a world which doesn't care whether you live or die, just that you produce value. Though, this being a general diagnosis applicable almost universally among many or most of us, its probably not of much use.
When we reconnected after that period, Josh had much more sadness about him. For a year, we both lived in Bay View and could visit each other by taking a ten minute walk past the big park and across KK. I think Josh was miserable for much of that winter, because he said as much, but for me the walks we took just talking and hanging out were anodyne; though I too was depressed in my life and far from productive or pursuing anything like a concrete plan. Sometimes we walked to Anodyne Coffee and marveled at the way people live their lives and what they consider important. The extra time I got to spend with him that year is a huge reward I was somehow given for I know not what good deeds. Josh brought much wonder and beauty into my life, as I know he did to pretty much everyone who knew him.
Josh thought life was a spiritual journey. The way he had of being concerned with things on a non-physical plane meant he was present for whatever was going on then and there. In light of this, the decision he made must be seen as a considered one. It may be true that suicides are impulsive acts, and that prevented from carrying it out, a person has a 4 out of 5 chance of living out their lives to old age. But statistics don't ask, "What were these lives like? Fulfilled? Happy? Meaningful?" At the same time, I know (as Josh surely knew) that there is an element of chance involved in all of this, and that life is fickle. It is always possible for everything to change at a moment's notice, for love to take you where you didn't know exists, for the shunned and ridiculed weirdo with his head in the clouds (yurodiviy of Russian folklore) to become the only person with anything resembling answers in a sudden reversal of everything anyone has ever known or taken for granted. He may have felt this gambling isn't "honest," or just that the odds aren't good. Or maybe it simply comes down to the ratio of pain to joy, and his reached an unacceptable level.
I'm not the first to note that all too often, it's the best ones that are taken away, that seem to stand no chance of making it in this world. I won't be the first one to say that this isn't right, and that it doesn't have to be this way. The facade was maintained, only a generation or two ago, that the goal of all our endeavors, all our industry, is for the betterment of the lives of men, the notion was that progress was human progress, concerned with the welfare of our species, if not the welfare of all life. There was serious discussion of what people would do with all their free time once menial tasks were mostly automated. Maybe it should have been obvious that this was a charade all along, and to some it probably was. Today, even the charade has been dropped: "progress" has come to mean the development of objects from simple into more complex forms, the total price of the stocks traded by robots and rich people on the NYSE has come to be an indicator of the fitness of our society, and no one talks about growth in terms of our minds or souls any longer. A society which, in the words of Aldous Huxley, is based on "organized lovelessness" does not deserve to exist. It is yet to be shown whether it can exist, in the long run.
Why we put up with it is another question. Clearly, many of us are simply not aware that any alternatives exist. Most people are convinced that the best they can hope for is a raise, a winning lottery ticket, "true" love, as opposed to the false kind. They've never seen a truly happy person in their life, have no idea what happy people do, where they come from, what kind of environment they inhabit, what they consider important. Most people wouldn't know what they're looking at if they did come across such a phenomenon. I have, and what's more, I've been one. A very faulty one, perhaps, but one nevertheless. By and large, this is a matter of the company you keep and are blessed with. The friendship I got to enjoy with Josh was part of the reason why I know what happiness for human beings feels like.
Kurt Vonnegut, speaking to an assembly of the American Psychiatric Association, said: "All of you, I am sure, when writing a prescription for mildly depressed patients… have had a thought on this order: 'I am so sorry to have to put you on the outside of a pill. I would give anything if I could put you inside the big, warm life-support system of an extended family instead.'" Whether they did have had such a thought is something only they know, clearly they wouldn't remain psychiatrists long if they not only believed such heresy but went around saying so. But I will take Kurt Vonnegut's wisdom over an assembly of psychiatrists any day: the point is that family—extended family—is an essential element we humans need to succeed, or to exist on any level but the most unfulfilling. Extended families don't treat each other as bosses, employees, competitors or customers. Extended families offer a human being the opportunity to love and be loved, to be a student and a teacher, to be comfortable in the knowledge that they are accepted for who they are and will always be, that while they may do something that can hurt or disappoint, they themselves will always remain a part of the group. By and large, no group of people, related or not, gets to live any longer in a manner that would allow their members to live, grow, and die in the embrace of the kind of community that we require to thrive, certainly no one I've ever met. If we're lucky, friends fill some of that space for some of the time—I consider myself about as lucky as anyone I know in this regard. Needless to say, it's a tall order to maintain the level of support we require in an informal group of this kind.
Here's hoping that the end of this dark age is at hand. When we finally manage to change the premises on which we've built this society, premises like man's mastery over the rest of creation and, by extension, some men's mastery over others, we may have a chance of ridding ourselves of the organized lovelessness that is the condition of such a society. When and if we do that, we will surely remember the ones who didn't make it as the victims of the bad old days, and some as the prophets who pointed the way towards sanity. Not that that can ever take their place.
I miss Josh almost daily, still. Living in a city which we spent so much time in together can't help but remind me of things we did, but even without outside triggers, I am the person I am today because of Josh. Sometimes I feel like with his passing, I am taking on his qualities. I got a puppy recently, and this has brought on all kinds of changes and new experiences which sometimes seem like deja vu, except not of something I've already lived, but that Josh did. I imagine him training June to "heel" and curb her prodigious energy as I do the same with puppy, or walking the Milwaukee river trails as we do almost every day.
Photos in this post except the top one are ©Josh Gilman.
Stay tuned for a page featuring Josh's poetry, fiction, travel writing, photos, and more.


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01. Aeon Sable - Aether
02. Amorphis - Queen Of Time
03. Atrium Carceri - Codex
04. Dimmu Borgir - Eonian
05. Behemoth - I Loved You At Your Darkest
06. The Eternal - Waiting For The Endless Dawn
07. MGT - Gemini Nyte
08. Primordial - Exile Amongst The Ruins
09. Khôrada - Salt
10. Immortal - Northern Chaos Gods
French ambient/black metallers Maïeutiste, who will release their self-titled debut album on 19th September via Les Acteurs de l'ombre Productions, just released a new track named "The Fall" which is taken from the album, accompanied with a video clip where the images are taken from Faust (1926) by F.W. Murnau. Previously unveiled track "Absolution" can still be heard over HERE. Now, give a listen to "The Fall" by pressing the play button in the YouTube player below. Link

subset: commoncrawl


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State Sen. Chuck Wiger
District 43
MN State Senator Chuck Wiger, District 43
Americans spend more money on prescription drugs than people in any other country.
"The only thing that you absolutely have to know is the location of the library."- Albert Einstein
"Education is the most powerful weapon which you can use to change the world." – Nelson Mandela
Many of us love the Minnesota State Fair. Whether it be 4H exhibits, the farm animals, midway rides, machinery hill, all types of food, great entertainment, information galore, the people and much more — this is the best fair in America.
"Commit yourself to lifelong learning. The most valuable asset you'll ever have is your mind and what you put into it." —Brian Tracy
"I thought about a graveyard. At the bottom of the sea. Of unmarked graves in Arlington. No, Freedom isn't free." —Kelly Strong
Every July 4, citizens across Minnesota and the country celebrate our Independence Day.
"I go to nature to be soothed and healed, and to have my senses put in order."
—author John Burroughs
The 2018 legislative session ended a few minutes before the constitutional deadline on May 21. Although there were some disappointments during the three-month session, there were some definite bright spots for our area.
"Twenty years from now you will be more disappointed by the things you didn't do than by the ones you did. So throw off the bowlines, sail away from the safe harbor. Catch the trade winds in your sails. Explore. Dream. Discover."
"Freedom has its life in the hearts, the actions, the spirt of men and so it must be daily earned and refreshed – else like a flower cut from its life-giving roots, it will wither and die." — President Dwight Eisenhower
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Starting School in 2020?
Dates for open sessions are now available!
If your child will be starting school in September 2020 then please come for a visit on one of our open sessions. You can see the available dates by downloading the poster below or by visiting our diary page.
To ensure that smooth running of these sessions we would ask potential parents to confirm their interest by telephoning or emailing the school office to inform them of which session they would like to attend.


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Thankfully hockey is still going
Nevada Appeal Betting Columnist
Wednesday night with Carolina up 3 games to 1 and playing at home, it sure looked like the Hurricanes would soon be crowned champions of the National Hockey League. The Stanley Cup was in the building and the ceremony had already been rehearsed. One more win and they would be carrying around the sacred trophy in front of their home fans.
But no! In the best and most important game of an exciting season, Edmonton scored a short-handed goal in overtime to spoil the party.
In hindsight, we should have expected it. Considering the excellence of this year's playoffs, it would only make sense that there would need to be at least one more great battle. Of the 81 postseason games so far, 39 were won by the road team, 20 went into overtime, and a remarkable 46 were decided by a one-goal margin. With two small market ex-World Hockey Association clubs duking it out, we should have known things would not come too easy for either team. Carolina management's decision to rehearse the ceremony just motivated Edmonton even more.
Prediction – In the wake of goaltender Dwayne Roloson's Game 1 injury, Edmonton back-up Jussi Markkanen has steadied the ship, which is amazing when you learn that the Finn last played in a game on March 1. With his help, Games 3 and 4 in Edmonton finished with final scores of 2-1. It would be heaven-sent to see a deciding Game 7 for the Cup on Monday, so the pick in tomorrow's Game 6 is Edmonton and Under.
If the Oilers do win Game 6, home ice will prove to be too much to overcome in Game 7, as Carolina will eventually prevail. In the last 29 occurrences, only Chicago in 1971 has blown a 2-0 Finals lead like Carolina had.
Note: No lame excuses left for true sports fans, as the games are now being televised on NBC.
Not knowing who won last night's game makes predicting the outcome of Sunday's contest more of a chore. But either way, with the pre-Finals pick of Dallas in 6, that means the Mavericks must leave Miami with a 3-2 series lead. If the Mavs won last night, the pick is Miami and Over in Game 5. If Miami won yesterday, the choice is Dallas and Over.
The NBA would just love to stretch the Finals to at least 6 games. Dallas will cover the point spread Tuesday, and the game will go Under.
The United States is in very deep trouble after its disappointing 3-0 loss to the Czech Republic. Now the U.S. must at least tie Italy tomorrow, and probably need to win in order to have a realistic chance of advancing out of its first round group.
It is apparent now that the United States definitely got hosed in the pre-tournament draw. Even though the U.S. was ranked No. 5 in the world, it was placed in the same bracket with No. 2 rated Czech Republic, a team that didn't lose a single match in qualifying. Putting the tradition of 3-time champion Italy in the same group made circumstances even more brutal. If the U.S. had switched places with Spain, it would have played Saudi Arabia, Tunisia and Ukraine, and easily advanced.
Prediction – In the last two World Cups, only one team has advanced to the second round after losing its first game. The United States should lose to powerful Italy, and will go home under excessive criticism.
Best bets in this weekend's games – Argentina, Holland, Mexico, Portugal, and Czech Republic.
If this event ends up anything like the women's softball championship, it should be very exciting. Only Oregon State returns from last year's field, and four teams are from the Atlantic Coast Conference.
Prediction – Cal-State Fullerton gave up the least runs in regional and super-regional play. Fullerton State defeats Rice for the title.


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Basic fibroblast growth factor (bFGF) is known to play a critical role in tumorigenesis of solid tumors. The importance of bFGF in hematological malignancies such as acute myeloid leukemia (AML) remains to be elucidated. Therefore, we determined bFGF protein expression by immunohistochemical analyses in bone marrow biopsies of patients with newly diagnosed, untreated AML. The expression of bFGF was significantly increased in AML patients [n = 81; median, 3.0 (interquartile range, 1.8–3.9) arbitrary units (AU)] as compared with controls [n = 18; 1.9 (1.5–2.3) AU]. The degree of bFGF expression did not correlate with microvessel density. bFGF/FGF receptor mRNA and bFGF protein were detected in different AML cell lines. To study autocrine growth stimulation of AML blasts, the AML cell lines HL-60, M-07e, and KG-1 were incubated with bFGF. A significant dose-dependent increase in proliferation and colony formation was observed. These effects were abrogated by the addition of a polyclonal anti-bFGF antibody. In conclusion, increased expression of bFGF in the bone marrow of AML patients seems to play an important role in the pathophysiology of AML by promoting autocrine growth stimulation of leukemic blasts.
bFGF 3 is the prototype member of a family of at least 20 structurally related, heparin-binding growth factors (1 , 2) . This factor is an important modulator of cell growth and differentiation under both physiological and pathological conditions. The biological activity of bFGF is mediated through a dual receptor system consisting of five high-affinity tyrosine kinase receptors, which display broad expression patterns (3, 4, 5) , and low-affinity heparan sulfate proteoglycans located at the cell surface and within the extracellular matrix. In this form, bound bFGF constitutes a reservoir of the growth factor that can be released in a regulated manner (6, 7, 8) . FGF-binding protein mobilizes and activates locally stored FGFs, and this can serve as an angiogenic switch molecule (9 , 10) . In addition to its extracellular effects, bFGF exerts intracellular effects that seem to be independent from tyrosine kinase-type receptors (2) . Moreover, bFGF is mitogenic for endothelial cells and stimulates endothelial cell migration and pericellular proteolysis (11) . Furthermore, there is evidence that the mitogenic and angiogenic effects are augmented by VEGF (12, 13, 14) .
Previous studies suggest a role of bFGF as a prognostic marker for solid tumors. In a multivariate analysis, it has been demonstrated that high bFGF levels are associated with poor prognosis in small cell lung cancer patients (15) . Recently, there is growing evidence that apart from this well established role in solid tumors, bFGF is important in the pathogenesis of hematological malignancies as well (16 , 17) . High serum bFGF levels were associated with poor survival in patients with non-Hodgkin's lymphomas (18 , 19) . In B-cell chronic lymphocytic leukemia, elevated intracellular bFGF levels were found in high-risk patients (20 , 21) , and the low-affinity bFGF receptor syndecan-1 (CD138) was detected on the surface of myeloma cells (22) . Patients with multiple myeloma had significantly higher serum bFGF levels than controls (16) , and response to chemotherapy was associated with a significant decrease in bFGF, indicating an important role for bFGF in multiple myeloma as well.
However, little is known about the role of bFGF in AML. bFGF was detected in HL-60 cells and in three of four fresh AML patient samples (23) . Furthermore, receptors for FGFs are expressed on some leukemic cell lines such as KG-1 and HL-60 (24 , 25) . This might suggest that FGF plays a role in leukemic hematopoiesis. Therefore, the goal of our study was to investigate the expression of bFGF in the bone marrow of adult patients with newly diagnosed, untreated AML and to investigate the potential role for bFGF in autocrine growth stimulation of AML blasts.
Bone Marrow Specimens.
Eighty-one consecutive patients (20–79 years old) with newly diagnosed, untreated AML were chosen for our study. This study population is an extension of the previously published cohort of 62 patients in whom the degree of bone marrow angiogenesis at presentation has been reported previously (26) . Eighteen unselected controls were taken from the initial group of 22 patients, which have been analyzed for bone marrow MVD as well (26) . These controls consist of adult patients (17–77 years old) with various diseases but with normal bone marrow morphology as demonstrated by cytological and histological analyses. From all AML and control patients, a bone marrow core biopsy (iliac crest) for histological diagnosis was obtained at presentation. After every core biopsy, a bone marrow aspiration was obtained through a separate puncture for cytological analyses. All patients had to give written informed consent to the study.
Immunohistochemical Staining.
The determination of the degree of angiogenesis was performed by immunohistochemical identification of microvascular endothelial cells with antihuman thrombomodulin antibodies as described previously (27) . For bFGF quantification, bone marrow specimens were fixed in paraformaldehyde, decalcified with EDTA, and embedded in paraffin. Serial sections (4-μm thick) of each sample were processed immunohistochemically for the expression of bFGF with rabbit polyclonal antihuman bFGF (sc-79; Santa Cruz Biotechnology, Santa Cruz, CA; working dilution 1:2000). Controls for immunostaining using nonimmune mouse IgG or rabbit IgG (sc-2025 and sc-2027, respectively; Santa Cruz Biotechnology) in substitution for the specific first antibodies were consistently negative (data not shown).
Immunohistochemical staining was performed by the alkaline phosphatase/antialkaline phosphatase double bridge technique (Dako-APAAP kit; Dako, Glostrup, Denmark). Briefly, tissue sections were deparaffinized in xylene and rehydrated in a graded ethanol series. Samples were pretreated to promote antigen retrieval in a microwave oven at 450 W twice for 7 min in 10 mm sodium citrate (pH 6.0; Dako). The primary antibodies were applied overnight at 4°C. Subsequent steps were performed according to the manufacturer's instructions. The fast red substrate (Dako) supplemented with 0.1% (w/v) levamisole was used for revelation of phosphatase activity (30 min at room temperature). Sections were counterstained with 0.1% (w/v) erythrocin solution.
Evaluation of bFGF Expression.
Immunostaining was simultaneously assessed by two independent experienced investigators using light microscopy. The investigators were blinded to the clinical characteristics of the patients and the bone marrow microvessel counts when performing the growth factor evaluation. Expression of bFGF protein was semiquantitatively assessed as described previously (28) . Results are reported as AU. In each biopsy sample, expression of bFGF was evaluated in two to three sections processed in independent immunostainings, and the mean value was calculated. To ensure the reliability of the quantification assay, marrow slides have been randomly selected during the study and reanalyzed with excellent agreement. A bone marrow specimen has been used as internal control in the study. Sections of this specimen have been repeatedly immunostained for the different antibodies and quantified by the two investigators at different times.
Blocking studies with the immunogenic peptide that elicited the bFGF antibody (Santa Cruz Biotechnology) demonstrated a substantial reduction of the staining level (≈80%) when preincubating the anti-bFGF antibody with the immunogenic peptide in a 100-fold molar mass of the antibody. This observation confirms the specificity of the bFGF antibody.
Cell Culture.
The human leukemia-derived cell lines HL-60 (promyelomonocytic leukemia), M-07e (megakaryocytic leukemia), and KG-1 (myelogenous leukemia) were obtained from the German Collection of Microorganisms and Cell Cultures (DSMZ, Braunschweig, Germany). The HL-60 and KG-1 cell lines were cultured in RPMI 1640 supplemented with 10% FCS (Life Technologies, Inc., Eggenstein, Germany) and 2 mm l-glutamine (Life Technologies, Inc.), the M-07e cell line was cultured in IMDM (Life Technologies, Inc.) supplemented with 20% FCS, 10 ng/ml IL-3 (Sigma, Taufkirchen, Germany), 10 ng/ml granulocyte macrophage colony-stimulating factor (Sigma), and 2 mm l-glutamine at 37°C and 5% CO2. All culture media were supplemented with 100 units/ml penicillin and 100 μg/ml streptomycin.
RNA Extraction, cDNA Synthesis, and RT-PCR.
Total RNA from AML cell lines was extracted using RNeasy total RNA system (Qiagen, Hilden, Germany) following the manufacturer's instructions. cDNA was synthesized for 1 h at 37°C, using 1 μg of total RNA, random hexamers, and Moloney murine leukemia virus reverse transcriptase (Promega, Heidelberg, Germany). bFGF and FGF receptor transcripts were amplified using Taq polymerase (Promega) on a Hybaid thermocycler (MWG-Biotech, Ebersberg, Germany) as follows: for 40 cycles at 95°C for 1 min, at 55°C for 1 min, and at 72°C for 1 min for FGF receptors; and for 35 cycles at 94°C for 1 min, at 55°C for 1 min, and at 72°C for 1 min for bFGF. The following primer sequences were chosen: bFGF primers (sense) 5′-AGAGCGACCCTCACATCAAG-3′ and (antisense) 5′-TCGTTTCAGTGCCACATACC-3′ (bFGF PCR product 223 bp); FGF receptor-1 primers (sense) 5′-AACCCCAGCCACAACCCA-3′ and (antisense) 5′-AAGCTGGGCTGGGTGT-CG-3′ (FGF receptor-1 PCR product 576 bp); FGF receptor-2 primers (sense) 5′-TCCTATGACATTAACCGTGTT-3′ and (antisense) 5′-TTTAACACTGCCGTTTAT-3′ (FGF receptor-2 PCR product 702 bp); FGF receptor-3 primers (sense) 5′-TTCGACACCTGCAAGCCG-3′ and (antisense) 5′-AGCAGGTCGTGGGCAAAC-3′ (FGF receptor-3 PCR product 629 bp); and FGF receptor-4 primers (sense) 5′-GCGGCGTCCACCACATTG-3′ and (antisense) 5′-GTCTGCACCCCAGACCC-3′ (FGF receptor-4 PCR product 502 bp). PCR products were separated on a 6% Tris-borate EDTA gel (Novex, Frankfurt, Germany) and visualized with ethidium bromide.
Western Blotting and Immunodetection.
bFGF was detected by Western blotting. A total of 1 × 107 cells were washed twice with ice-cold PBS with protease inhibitor mixture (Sigma). After brief centrifugation, the cells were resuspended in a small volume PBS containing 0.5% SDS followed by an incubation for 5 min at 95°C. Protein extraction was done by sonification of the pellet. Protein concentration of the lysate was determined by BCA assay (Pierce, Bonn, Germany). Equal amounts of protein (50 μg) were subjected to a 12% SDS-PAGE under reducing conditions and electroblotted overnight at 30 V onto a polyvinylidene difluoride membrane (Amersham Pharmacia Biotech, Freiburg, Germany), using a towbin transfer buffer in a minitrans-blot apparatus (Bio-Rad, Munich, Germany). Blocking of the membrane and probing with a polyclonal bFGF antibody (Santa Cruz Biotechnology) were performed according to the Opti-4CN protocol from Bio-Rad. Reactions with the bFGF antibody were visualized using an enhanced chemiluminescence kit (Bio-Rad).
Cell Proliferation Assay.
To study the effect of the growth factor bFGF on the proliferation of the leukemic cell lines HL-60, M-07e, and KG-1, the cells were plated in a 96-well plate (5 × 104 cells/well; Nunc, Wiesbaden, Germany). Before plating, the cells were starved for 24 h with the corresponding medium, i.e., the HL-60 cells with RPMI 1640 with 2.5% FCS, the KG-1 cells with IMDM with 5% FCS, and the M-07e cells with IMDM with 10% FCS, interleukin 3, and granulocyte macrophage colony-stimulating factor. Thereafter, we added 10 μl of the required bFGF concentration (final concentration in the cell suspension: 0–25 ng/ml; Boehringer Mannheim, Germany) with or without a polyclonal anti-bFGF antibody (25 ng/ml, AB-233-NA; R&D Systems, Wiesbaden, Germany) in triplicate to the cells. After 18, 24, and 48 h, the cells were harvested and counted under the microscope in a Neubauer hemocytometer. The cell viability was monitored by trypan blue dye exclusion.
Colony Assays.
For evaluation of bFGF-dependent colony growth of the HL-60 cell line, methylcellulose assays were performed by using a modification of a technique described previously (29) . Briefly, HL-60 cells were plated at a density of 3 × 104 cells/ml in methylcellulose agar consisting of methylcellulose (Sigma, Deisenhofen, Germany), Difco agar (Agar noble; Difco, Detroit, MI), IMDM (Life Technologies, Inc.), 2.5% FCS, and β-mercaptoethanol (Life Technologies, Inc.). This incubation mixture was vortexed thoroughly and kept in the dark at 37°C for 20 min. One ml of this mixture was plated in a tissue culture dish (Nunc). The number of cells finally seeded/dish was 1 × 103. To each plate, we added the required concentration of bFGF (final concentration: 0–500 ng/ml) and anti-bFGF antibody (final concentration: 100 ng/ml, 100 μl/plate). The colony numbers were determined by using an inverted microscope after an incubation period of 10 days at pH 7.2, 37°C, in an atmosphere of 5% CO2 and high humidity.
Data are presented as individual data plots or as medians, interquartile ranges (low quartile − high quartile [LQ − HQ]), and ranges. Differences in expression of bFGF between AML and control groups, as well as between AML patients with high and low microvessel densities, were analyzed by the Mann-Whitney rank-sum test for independent groups. Statistical significance of overall differences between more than two groups was analyzed by the Kruskal-Wallis one-way ANOVA. Correlation between variables was assessed by the Spearman rank correlation coefficient (rs). Two-sided Ps < 0.05 were considered significant, and corrections for the number of comparisons (Bonferroni test) were performed when required.
The expression of bFGF was evaluated by immunohistochemical staining in bone marrow core sections of 81 AML patients at first diagnosis. Patient characteristics are depicted in Table 1 ⇓ . The results from these AML patients were compared with the degree of bFGF protein expression in bone marrow biopsies obtained from 18 patients with different diseases but with a normal bone marrow morphology. In the cases of the Hodgkin's disease, the non-Hodgkin's lymphomas, and the kidney carcinoma, the bone marrow was histologically not involved by the underlying disease (Table 1) ⇓ .
The bFGF antigen was consistently detected in every bone marrow specimen from AML, as well as control patients. The staining intensity in the AML bone marrow varied from weak to strong, and the location of the immunoreactivity was extracellular as well as intracellular, as shown in Fig. 1A ⇓ . Nearly 60% of the AML patients exhibited extensive bFGF staining, whereas 20% were weakly stained for bFGF. In contrast to the AML specimens, the control bone marrow samples displayed a heterogeneous pattern of bFGF staining throughout the cellular areas (Fig. 1B) ⇓ . Both in AML and control specimens megakaryocytes were stained with anti-bFGF antibodies as well. However, these were easily recognized by their characteristic size and morphology. Beside the megakaryocytes, the endothelial cells were weakly or moderately stained for bFGF. The bFGF protein staining scores of the 81 bone marrow specimens from AML patients ranged from 1.0 to 8.5 AU with a median value of 3.0 AU (LQ-HQ: 1.8–3.9), whereas control bone marrow samples (n = 18) showed significantly weaker bFGF protein staining (median, LQ-HQ: 1.9, 1.5–2.3 AU; Mann-Whitney test, P = 0.04; Fig. 2 ⇓ ).
The median (LQ-HQ) staining scores for bFGF in relation to the AML FAB subtypes are shown in Table 2 ⇓ . Interestingly, statistical analyses did reveal a significant difference in the expression of bFGF in AML subtypes (Kruskal-Wallis test, P = 0.037). Beside the M3 subtype (three samples only), the M4 subtype showed the highest bFGF values. The staining scores of the M6 subtype were in the range of the controls (Table 2) ⇓ .
Patients < 60 years showed significant higher bFGF immunoreactivity than patients > 60 years (median, LQ-HQ: 3.4, 2.4–4.9 AU versus 2.3, 1.6–3.5 AU, P = 0.037). However, there was no correlation with gender or the degree of leukemic blast infiltration.
From each bone marrow specimen, adjacent sections to those processed in the present study were immunostained with specific markers of endothelial cells (antihuman thrombomodulin antibodies) for the assessment of MVD. The results for MVD of the subgroup of 62 patients have previously been reported (26) . The median MVD in the 81 AML patients was 24 (LQ-HQ: 20.4–28.3) microvessels/×500 field and 12.2 (10.6–14.3) microvessels/×500 field in the 18 control patients, respectively. Thus, the MVD values for the presently larger group of AML patients and the subgroup of the control population were not significantly different from those reported previously (26) . The expression of bFGF in the bone marrow was not related to the MVD levels in the group of AML patients, as well as in the total study population (81 AMLs and 18 control patients). Bone marrows of AML patients with strong angiogenesis (76–100% quartile of the population) showed no different staining scores for bFGF than AML marrows with low MVD (1–25% quartile; marrows with >28.8 microvessels/×500 field versus marrows with <19.2 microvessels/×500 field: bFGF, 2.2 versus 2.7 AU, P = 0.401; Mann-Whitney test). Furthermore, we found no correlation between bFGF expression in the bone marrow and the degree of MVD in the entire cohort (rs = 0.122 for 81 AMLs and 18 control patients, P = 0.285).
bFGF and FGF receptors mRNA was detected by RT-PCR in the different AML cell lines HL-60 (FGF receptor-1, FGF receptor-2, and FGF receptor-4), M-07e (FGF receptor-2, FGF receptor-3, and FGF receptor-4), and KG-1 (FGF receptor-1; Fig. 3 ⇓ ). Obviously, the type of FGF receptor expression pattern differed between various cell lines. Furthermore, bFGF protein expression was demonstrated by Western blotting in all three cell lines (Fig. 4) ⇓ . To study bFGF growth stimulation of AML blasts, we investigated the effect of exogenous bFGF on the proliferation of these human leukemia cell lines. bFGF induced an ∼2-fold increase in proliferation of all cell lines in a dose-dependent manner (Fig. 5) ⇓ . Furthermore, the stimulatory effect could be inhibited by the simultaneous addition of neutralizing polyclonal anti-bFGF antibodies (Fig. 6) ⇓ .
To further evaluate the role of bFGF on the growth of leukemic blasts, we studied the effect of this cytokine on the colony formation of the HL-60 cell line. Exogenous bFGF dose dependently promoted the degree of colony formation ∼2-fold (Fig. 7 ⇓ , Kruskal-Wallis test, P < 0.0001). This stimulatory effect was nearly completely abrogated by polyclonal antibodies against bFGF (Mann-Whitney-Test, P < 0.0001).
Recent studies have shown that increased angiogenesis is a common feature in the bone marrow of AML patients (23 , 26 , 30 , 31) . Furthermore, there is growing evidence that the growth factor VEGF and its receptors VEGFR-1 and VEGFR-2 play a key role in tumor neovascularization of hematological malignancies (27 , 28 , 32, 33, 34) . Beside VEGF, bFGF is a potent angiogenic inducer that may act synergistically in vitro and in vivo (11 , 12 , 14 , 35 , 36) . Thus far, only few data about the importance of this growth factor in the pathogenesis of AML have been reported.
The current investigation, based on the immunohistological analyses of bone marrow core biopsies of a large cohort of patients, has clearly documented a significantly increased expression of bFGF in leukemic blasts of patients with newly diagnosed, untreated AML. Until now, there are only a few studies concerning bFGF or FGF receptors in AML, mostly done with cell lines obtaining conflicting results (23 , 25 , 37, 38, 39, 40) . One group was able to detect bFGF mRNA in the HL-60 cell line (38) , and others found a bFGF message in the HL-60 cell line, as well as in leukemic blasts in 3 of 4 patients (23) . However, by the use of a semiquantitative scoring system, our study is the first that demonstrates unequivocally a significant increase of in situ bFGF protein expression in the bone marrow of many unselected patients with AML compared with controls.
Other studies investigated the role of bFGF in AML and myelodyplastic syndrome by measuring bFGF serum or plasma levels or soluble bFGF in supernatants of primary cultured AML blasts (30 , 41, 42, 43) . One group found significantly increased serum bFGF levels in patients with acute and chronic leukemias and myelodyplastic syndrome (30 , 43) . In contrast to these and our results, however, two of these analyses did not reveal elevated serum or plasma bFGF levels. Thus, the authors argued against a predominant role of this mediator in these malignancies (41 , 42) . However, these conflicting results are not surprising because elevated levels of FGF are rarely found in biological fluids because of its strong association with cells and the extracellular matrix (44) . This pool of FGF constitutes a reservoir of the growth factor that can be released and activated, e.g., by heparanases or by FGF-binding protein in a regulated manner (1 , 9 , 10) . Moreover, by measuring serum levels of bFGF, the high molecular weight forms of this mediator would most likely not be detected because of their strict intracellular location (45) . Thus, the advantage of quantifying bFGF by immunohistochemistry is its ability to detect all bFGF isoforms. In contrast, by measuring serum bFGF exclusively, the low molecular weight isoforms of this growth factor that are not cell or matrix bound are detected. This could result in underestimation of the role of bFGF in AML and could explain the previous findings that serum bFGF levels were not elevated in patients with this disease (41 , 42) .
bFGF is known as a potent activator of endothelial cell proliferation and can thus stimulate angiogenesis. However, the bFGF staining level did not correlate with the microvessel density of the evaluated AML patients, neither for the entire group nor for subgroups (FAB subtype, age, gender, and blast infiltration). An explanation for this unexpected finding may be that bFGF possibly does not act directly in stimulating angiogenesis in AML. First, whereas VEGF receptors are up-regulated and readily detected on endothelial cells of newly formed blood vessels in vivo, this does not appear to be the case for FGF receptors (46) . Second, FGFs are stored in the extracellular matrix bound to heparan sulfate proteoglycans and can be mobilized by secretion of heparanases or bFGF-binding protein from tumor cells (9 , 10) . Because of this complex biology of bFGF, the effect on neovascularization is hardly to predict. Therefore, the lack of a direct correlation between in situ bFGF expression and MVD is not surprising.
The fact that bFGF expression levels were not related to MVD might argue against the hypothesis that bFGF secreted by AML blasts support leukemic cell growth by increasing microvessel density (paracrine mechanism). Therefore, we pursued autocrine growth stimulation mechanisms in cell culture assays. bFGF/FGF receptor mRNA and bFGF protein were expressed in all investigated cell lines (HL-60, M-07e, and KG-1). This is in line with other groups that detected at least one FGF receptor on HL-60 (39 , 40 , 47) . In contrast to these and our results, one group, however, could not find bFGF or FGF receptors on this cell line (25) . Moreover, we were able to demonstrate that exogenous bFGF (18-kDa bFGF) stimulates the proliferation and colony formation of various AML cell lines in a dose-dependent manner, thus supporting our findings that functional FGF receptors are present in these cell lines. However, we did not observe a significant difference in the bFGF-induced response among the various cell lines. Thus, the effect of bFGF seems to be independent of the FGF receptor expression pattern in the specific cell line. The specificity of this effect is underlined by the observation that the stimulation of proliferation and colony formation was inhibited by the addition of a polyclonal antibody against bFGF. Thus, the bFGF/FGF receptor pathways seem to play an important role in autocrine growth stimulation of AML blasts.
The observation that the addition of the anti-bFGF antibodies alone (without exogenous bFGF) did not significantly reduce the growth of the leukemic cells seems to argue against a formal autocrine loop. However, the lack of such an inhibitory effect may easily be explained by intracellular bFGF activity not accessible for the neutralizing capacity of the antibodies (intracrine loop; Ref. 45 ). Furthermore, the source of bFGF in the AML bone marrow may additionally stem from the bFGF pool bound to the extracellular matrix. Thus, AML blasts could release bFGF from this pool by secretion of heparanases or bFGF-binding protein, ultimately leading to their own growth stimulation.
In conclusion, bFGF is overexpressed in the bone marrow of AML patients. The promotion of proliferation and colony formation of AML cell lines by exogenous bFGF points to an important role of autocrine mechanisms by this growth factor in the pathophysiology of AML.
We thank Drs. Gabriele Köhler and Horst Bürger (Gerhard Domagk-Institute for Pathology, University of Münster, Münster, Germany) for their advice and assistance in performing the immunhistochemical studies.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
↵1 This study was supported by Deutsche Forschungsgemeinschaft Grant Me 950/3-1.
↵2 To whom requests for reprints should be addressed, at Department of Medicine/Hematology and Oncology, University of Muenster, Albert-Schweitzer-Strasse 33, D-48129 Muenster, Germany. Phone: 49-251-83-47594; Fax: 49-251-83-48745; E-mail: mesters{at}uni-muenster.de
↵3 The abbreviations used are: bFGF, basic fibroblast growth factor; FGF, fibroblast growth factor; VEGF, vascular endothelial growth factor; AML, acute myeloid leukemia; AU, arbitrary unit(s); IMDM, Iscove's modified Dulbecco's medium; FAB, French-American-British; MVD, microvessel density.
- Received March 13, 2003.
- Revision received August 5, 2003.
- Accepted August 19, 2003.
- ©2003 American Association for Cancer Research.


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Hi, everybody. I'm Dr. David Granet and
welcome to Health Matters. It's estimated that
up to 66% of the American population is
currently overweight or obese. If you're not talking
about it right now, you probably were
just a few minutes ago. Recently, there's been a
new study that talks about the influences
of the environment, your friends
and your family. I'm going to talk about
which is more important on how you look and how
much weight you have. To help us get through this,
we have the author of that study,
Dr. James Fowler, who's an associate professor
of political science, and we'll point out that his
doctorate is a PhD, what we call a real doctor. We also have
Dr. Mike Gottschalk who is a professor
of pediatrics and Chief or "El Jefe" of pediatric endocrinology
here at the University of California
San Diego as well. We have you both
here because this crosses disciplines
into effecting everyone. Well, we've been
talking about it before we started the show. Everywhere you turn,
there is something about the study
that you guys recently did and it's just amazing
looking at the social network and how that
can affect weight. Can you give us
a quick summary? And then we'll delve
into some of the details. Sure. So we got some data from the Framingham
Heart Study which is this really
long-running study. It started actually
in the late 1940s and we've learned
a lot of what we know, for example, about
the relationship between heart disease
and smoking from this study. So this study is going
on today even still. And starting in the 1970s,
the study started keeping records on peoples'
friends and family. So we actually got
a grant to map the social network
of the people in the study so that we could see
who was friends with whom and what family members
people had in the study. And because it was
such a small group there in Framingham, a lot of these people
connected up to one another so that we could
see the influence of one person's weight gain on another person's
weight gain. Well, you say small,
but it's like 12,000 people. Yeah, 12,000 people. What I mean by small
is it wasn't a study of people all
around the country. It was a single
community so that, when people mentioned
who their friends were, they were also likely
to be members of the study. And you had information
about how much they weighed? Absolutely. Again, this is
a gold standard study and they actually
had doctors weigh them every two to four years. So we looked across
the seven different exams, 32 years, to see what
happened as one person gained weight to their
friends and to their family. What we found was
really stunning. We thought we would
find something, but we didn't realize
the effects would be so large. We found that,
if your friend becomes obese, it increases your own risk
of obesity by 57%. But what if your
family member is obese? Also, we found, if your
siblings become obese, it increases your risk
by 40% and, if your spouse becomes obese,
it increases your risk by 37%. See, I'm still shocked
by that because it would seem to me that your spouse
who you're with every day would have more of an impact
on you than a friend, but it was not that way. It's funny you should
mention that because, when we first started
doing the modeling, we looked at that result
and we thought nobody is going to believe this. You know, my wife, she
has less influence on me? I mean, heck,
my wife makes the meals. That's right, that's right. Sometimes the husbands
make the meals, but spouses, they spend
a lot of time together. So we looked more carefully
at the friendship data and the sibling data
and what we found in that data is
that same-sex relations were much more important
than opposite sex relations. So men apparently
looked to men and women looked
to other women more than to members
of the opposite sex. So while spouses spend
a lot of time together and on average are
really good friends with one another, they're also
members of the opposite sex. So those two factors will
work against one another. And my wife told me
that many years ago, that she doesn't dress
for me or the other men. She's dressing
for the women because they all look
at each other. So it made sense
to me because I've been educated on
that aspect already. Now when you heard
the results of this as a clinician
dealing with weight issues, especially in children,
were you surprised or did you expect
the family relationships to be more important? Well, I think, with children,
we're in a little bit more of a unique situation
because the parents and the family have
a tremendous influence on the child. For example, the parents
buy the food, the child has some
access to it. So some of
the decision-making that goes on in terms
of lifestyles are really controlled
still by parents. But we were surprised
because I think this is a novel paradigm
that really hasn't been explored before. And as we're trying
to go forward and trying to prevent obesity, as well as potentially
come up with regiments to treat obesity,
you really have to understand what are all
the variables in terms of barriers and
what's driving this. If we don't
understand that, then no matter what
we come up with a scheme, we're not going to be
very successful with. I mean, some of the
impacts on this, I was thinking
about as a physician on trying to impact
someone to get them to start an exercise program
or something. One of the things
that was, I think, the most powerful effect
in this study that you wrote was that,
if two people said each other were friends,
the number skyrocketed on the effect. Absolutely. So these forms that we collected
the information from asked people
to name a close friend who would know where you lived
two to four years from now. So we had three different
kinds of relationships. So I could name
you as a friend so we could see your effect
on me or my effect on you, or we could both name
each other as a friend. It makes sense that, if we
name each other as a friend, that that's probably evidence
of a stronger relationship and we found there a much,
much stronger influence between mutual friends
than between friends where only one person
named the other person. The other really
interesting thing, in these association
studies, we really have
evidence of causality, but what we found was, if I name you as a friend
and you become obese, it increases
my risk of obesity, but not the other way around. So this is just an effect
of people that we esteem, people that
we name as friends. You may be sort
of blissfully unaware of my existence if I name
you as a friend, right? Then I'm not going
to have an impact on you. So the fact that
the influence seemed to flow in one direction is,
we think, really strong
evidence of causality. Which is amazing. Again, going back
to the actual now putting that into effect,
I'm thinking about trying to change someone's behavior and you're talking
to them in the office, but their friend's obese and the friend's not
sitting there with you and that friend has
a very powerful effect. It almost changes
the paradigm. It does, and I think
we were talking before. One of the questions comes
is how does influence occur? Is it that the person
is looking for acceptance of the change
in their weight, and they're going
to be satisfied with the fact that
they're gaining weight and not want to make a change? If their friends,
though, perceive that that's not what
should be happening, then trying to get them
to influence the change is going to be
really important. So it becomes difficult,
though, because you can't get friends over distances
to maybe go to the gym unless they have a webcam
and they can show each other exercising at the same time. But I think there
are other strategies that you can involve within
sort of local friends and close friends and sometimes it's
already been done because you look at–
there's a TV show in which they try to get
everybody to lose weight at the same time and they
make it a competition. There are organizations
where, you know, at work, they said, okay, as a group,
we're going to lose 80 pounds, so I think there's
a very social networking going on and that's
how this sort of pull and tug that you can
bring people along together and maybe more effective
than trying to just look at individuals in isolation. Absolutely. Well, that's an interesting
way to discuss even spending money from
a public health standpoint is influencing the social
network at a workplace rather than the individual
in front of you. Absolutely, and another
interesting thing about the study,
because we have these maps of the social network,
we not only knew what was happening
between friends, but between friends' friends. So you may have a friend
and I don't know that person and, if you
and I are close friends, that person's weight
also affects my weight. In fact, it extends to your
friends' friends' friends, three degrees of separation
into the network. So people that
you've never met, you have an influence
on them and they have
an influence on you. Somehow whenever I drop my son
off at elementary school, there are all these people who
are in their workout clothes. You start to see–I looked
at the world differently after reading your report and
looking at these influences that are all around us
of who we respect and who we are friends
with and what they look like in a way that I never
would have before, especially in
the application to medicine. I still find it amazing
what you found. Though it's interesting
because we found the what, but we still don't
know the why, right? So there's is this association
that does appear to flow in one direction,
but why is the case? Is it because of acceptance of
larger body sizes over time? Is it because of shared
norms about eating, shared norms about exercise? Those are things that
we really need to explore in order to be able
to give better advice on what these
interventions should be when you get your friends
and family involved in your own health behaviors. And we clearly
want to start this early. I mean, we want people
to have good behavior early. You're involved
with the PACE program. Correct. Could you tell us
a little bit about that? So this is a study trying
to make changes in lifestyle both in respect
to eating and exercising. We're working with children
who are at risk for developing
Type 2 diabetes. So they're overweight,
they may have a strong history
of Type 2 diabetes in their family, usually
there are certain ethnic minorities
such as African Americans, Hispanics in this community,
Asian Americans. What we want to do
to see if through behavior modification,
but hook the adolescent to something that
they use commonly, and that's the Internet
or cell phones. So the idea is that they go to
a website on a weekly basis, they log in and they
have been asked to select goals that
they're going to make in terms of diet
and exercise. For diet, we use what's called
the Stoplight Diet so foods are broken down
into reds, yellows and greens, not the color of the food, but these are
not healthy foods, these are better selections… The different curries. So even though peas are green, we won't get a lot of kids
going to that direction. And what we'd like to see is,
when they enter the study, we take inventory of
what their typical diet is and their selections and
their preferences and then, at the end of the year,
to see if we can shift from more out of the reds
more toward the yellows and greens and,
conversely, trying to get them to increase
their daily physical activity. So they wear pedometers
which keeps track of how many steps
they're taking, and the goal is over time
at the increased amount of physical activity. So the behavioral part
comes in is that they go on, they log onto a website,
they can see. They select their goals. It's not that
we're prescribing what they have to do. They have choices to make
based on what their preferences are,
which I think is really the only way that
you're going to affect change in the individual. And then they get feedback
because they see the changes they made over each week,
they get rewards. We use a lot
of music downloads because we're dealing
with adolescents. This is social networking. Do they get to talk
to other kids who are living through this
at the same time? One of the arms is, not only do they have
this internet access, but they come back for
sessions with other kids within that same group,
so they interact. And we bring parents, too,
so the parents have a piece of this as well. This, again, goes back
to influences and, certainly from my
own clinical experience, I think the children that are
most successful losing weight is when we get the parents to
lose weight at the same time. Because if the parents
see changes and they're feeling better
about themselves, then they're going
to just pull that kid out the door with them and
go for a walk with the dog. That's how that's how
they effect change. So when the groups
come back together, it's been very
interesting to see because they share
their experiences and see what's
successful for them, what's worked for them,
what hasn't, what are their challenges,
what obstacles do they still have and how
do they perceive themselves. You started this program
before the study that Dr. Fowler had done
and came out, but you were hitting on
the same sort of principles of the influences. I think the influences
in his study are even different
than what we considered typical influences because I think
certainly with adolescence, peers are very important. You know, this is a time
where they're moving away from their parents and trying
to develop independence, so their peer network
is really important. It may not always be,
though, that they consider all their peers are
sort of their best friends, but they survive under
this peer pressure. That's a little bit
different than I think what you're describing,
but certainly this has to also exist
for the adolescents as well and it's important
to realize that so we can tap into that and
use that to our advantage. When I was reading
about the PACE program, one of the things that hit me
was that the obese adolescent may become antisocial
or isolated and then their
social network is reduced to their family, which
becomes their influence. Then I started thinking,
well, getting their parents to lose weight
is obviously important, but their parents aren't
going to lose weight unless they have a friend
whose influence– You know, you start trying
to do those dominoes and making them fall, of
trying to impact all that, you got this kid that
you're trying to help who's at risk for diabetes and you want to get
the parents to go, but the parents
are going out for barbecue every night
with their social group that plays cards
together or something. How do you make those
changes and it starts to become a pretty big issue. I just want
to emphasize something about this particular issue. It certainly is the case
that obesity is associated with social isolation and
a lot of people, I think, interpreted the results
of our study to be that, if you have a friend
who becomes obese, that you should stop
being friends with them. That's not at all
the message of our study. We studied existing
friendships, right? So there's nothing
that you can infer from our study about,
you know, getting rid of your friend
or getting a new friend who might have healthy
eating behaviors. We looked at the
existing network, but there's this huge
literature on social support that shows that,
when you have more friends, you're healthier. You get more support, you
feel better about yourself. There's sort of a number
of causal mechanisms that cause us to
become healthier when we have more friends. There was so much
kind of controversy on this point
with the study that I actually went
back to our data and looked to see
what happened to people who got rid of friends
once they became obese. So you actually had the data
so that, if their friend changed weight
and gained weight and then you looked back
the next visit and they're no
longer friends… – That's right.
– What happens to them? It increases the risk
of obesity, yes. So getting rid of the friend
actually increased their risk. That's right. So on balance, you may
gain something from having a set of
friends who are engaged in healthy behaviors,
but what you lose from losing the friend
is actually much worse. So the last message
you should take from this study is
to get rid of any friend. So the best message
might be you and your friend together
lose weight. Absolutely, and I think
that a lot of people already understood
this, right? I mean, some people
reacted to the study, oh, that's really neat,
and others reacted, well, duh. I knew that the best way
for me to be able to change my own behaviors
is to get my friends and family involved. I mean, you have
WeightWatchers. In other domains, you
have Alcoholics Anonymous. These are groups that
have already understood very well that social networks
are really the core for a successful change
in your lifestyle. But no one had looked at it
quite like you had before. We just didn't
have the data before. Now we have the data and we can
really confirm our intuitions. So there are a lot of people
who spend time watching TV. Often adolescents
fall into that category. There are role models
that fall into TV. There are from MTV videos to
people we see on television. How do we fit that impact
into what the social norm is or behavior for people? It's not your friend? I think that people sort of
think about them that way, but they're not truly friends. Where does that fit, a role of
television playing in weight? Good question. One of the things that our
study really indicates is that you have to be
very good friends with somebody in order
for there to be an effect. So, for example,
we looked at the effect of immediate neighbors
and there was no effect. So that can be someone that
you actually see frequently, but you're not necessarily
very close to them. And if they become obese,
it has absolutely no impact on you. Also, the sort
of the stronger… So if my neighbors are
listening, they can… That's right, so they can go
ahead and eat the extra steak. They can breath easy. But the idea is that
this has to be someone that you're very close to, close friends,
close family members. So the idea
that television watching or sort of these
relationships on the Internet are going to influence this. You know, seeing models on TV
or the thousands of people you're connected to
in Facebook, those people are
not going to matter. The people that are
going to matter are going to be the people
that you're deeply and closely socially
connected to. Can you compare that effect
to other effects? In other words, eating habits,
activity of lifestyle. Is it all tied in or is this
just one piece of the puzzle? We certainly expected them
to be tied. Actually, you might know
a little bit more about this than we do because
we've really just tried to state what the association
is between different individual's weight. I do know that the next thing
we're going to be studying is what foods people
are eating in this network. So we just got a grant
to do this and they took a food
frequency questionnaire where they asked
detailed questions about what people ate. So just as a tongue
in cheek example, we drew the banana-eating
network. How many bananas
do you eat a week? But this is going
to obviously feed into– you know, we can categorize
these foods as green, yellow and red. I can imagine green circles,
yellow circles and red circles all sort of connected
to each other and you can see the extent
to which good eating behavior or bad eating behavior flows and how it's related
to obesity. And you probably predict
that those food color networks would match up with
the friendship networks and obesity.
I mean, they overlap. That's certainly
what we expect, but that work
has yet to be done. And it goes together with
what you're trying to do with PACE and the other
work that you do trying to change
that behavior and where to get
the levering to do it. I think what's
interesting about this study, again, is that these
sort of transitioned over distances and,
like you said, you can be three or
persons removed. So it's a little
difficult to imagine that it's going to be
just how you eat because how would
that fourth person really know how the
first person is eating? It's sort of like
the old telephone game when we were younger kids
and your whispered message was totally different
at the end. Right. So as you start moving
down the links, I think you start
to lose some of the effect – and some influence.
– Absolutely. But I think it still
goes back more to, as you talked about,
friendships and how people perceive each other
and acceptance of their perception. My wife's a runner,
so she's friends with other people
who run who are friends with other people who run and that's the way
I looked at it, that they have
common interests that lead them
in certain directions. We'll see how it holds up. That's probably true. I should emphasize the fact
that the effect gets smaller as you get further away. So by the time
you're four degrees removed, there's not
an effect, right? So the strongest ones
are the ones we're directly connected to. So it is like
the game of telephone. Eventually, you know,
it's noise. I had a couple of myths
that I made sure I wanted to ask you
and you answered two of them already. The third one I had was,
is obesity contagious? Is it infectious? Or is the idea of obesity
what goes on? Is there a virus that they're
spreading amongst friends? I think the ideas
are infectious. So we think
this is about norms. One of the aspects of the study
that was really interesting is that, when
we looked at friends who were thousands
of miles away versus friends
who lived very close, the effect was pretty
much the same size. So this indicates
that it's not because we're going
running with a friend or we're eating
with a friend. These are really
about us exchanging ideas about what healthy eating
and healthy exercise behavior is and what
a healthy lifestyle is. I mean, these are people that
you could see once a year and they still have
a tremendous effect on who you are. It's very impressive when
we talk about it this way. He's getting grants
to do all this. He's getting a lot
of money to do all this. How important is it that we
talk about obesity and weight? Well, it's tremendous
because the change in the prevalence of obesity
has just been staggering in the United States. The prevalence has
doubled to tripled in certain populations. Certainly, adults now, 60%,
over two-thirds, people are considered
to be overweight and a third are obese
and the children's prevalence are just trailing behind at just about
a decade beyond that. As you're well aware,
there are so many medical complications
to obesity starting from developing
insulin resistance and causing potentially the
increase of Type 2 diabetes. As an pediatric
endocrinologist, when I started 17 years ago, I never saw a child
with Type 2 which we typically
associate with adults. Now 25% of the children
we see with new onset have Type 2 diabetes. And that's really
related to weight? It's really related
to weight because this has changed too rapidly
to be a genetic influence. It's clearly an environmental
influence in change. It's estimated right now,
for example, that every child
that's born today, if the prevalence
of obesity continues at its current
escalating rate, that a third
of those individuals will develop diabetes by
the time they're adults. Wow. A third? A third, so there are
quite staggering figures. Not only do we see
within the terms of the realm of diabetes,
but children are developing a disease
or fatty infiltration of the liver and
that can actually go on and develop cirrhosis, so there's a much
higher prevalence of this disorder now. We see a lot of orthopedic
problems because of obesity. Sleep apnea is another
significant problem that we're seeing, and this is being parlayed
into the adult world as well. Now you're doing some
other work on smoking and drinking and happiness? Yeah, yeah, so smoking,
we just submitted a paper and one of
the interesting things there is you can look at
the cluster sizes of smokers. So how many smokers
are sort of connected to each other? The incidence of smoking
has dramatically decreased over the last 30 years,
so in some sense, it's sort of the mirror image
of the obesity epidemic. But the size of these clusters
has remained the same, the average size. What that means,
if those two things are happening at once,
is that whole groups of people are
quitting together. So this is sort of the main
sort of interesting point. It's not people sort
of at the edge of a social network
that are quitting. It's whole groups of people. One person quits,
then everybody in the group quits. But that's proof of concept
in essence of the PACE program and
these other programs being able to get groups
together to make an impact, reversing that effect. Right, assuming that
the same mechanisms work for smoking
as they do for obesity. We hope that's the case. You know, as a doctor,
again, is there anything good about smoking? Not that I can think of. Nothing good about smoking, and is there anything good
about being obese? No. I mean, these are
lifestyle changes, these are things that people
can do for themselves. If somebody came
to your office and there was things
you could do to help them to lose weight
and you didn't, they'd be furious with you. Yet there are things
that people can get involved themselves
to make a difference, and smoking is like that,
obesity is like that. And if these networks continue
to hold up that way, you may have helped
us identify– and you've already
been working in that world– but even sharpen
our tools to influence those networks to get
positive behaviors. I certainly hope so. I mean, that's a big
motivation of mine. I have members of my family
who are afflicted with obesity and
I would love it if something that I did–
so often it's up in the sky– but if something I did
actually had a positive impact on their lives, I would
just be thrilled. So you have to take a moment
and tell us about the happiness study. Okay, yes. We also are
studying happiness. They gave this
depression questionnaire to individuals in
the Framingham Heart Study and part of that
questionnaire are several questions
on happiness. And what we're finding
there is that happiness spreads from person
to person as well. This is really interesting
because we already know that there are
these short-term effects of happiness. If I smile, it increases
the chances that you'll smile
and vice versa. It is locally contagious. But there have been
these other studies that show that
happiness is fleeting. So, for example,
if you win the lottery, you'll increase the amount
of happiness that you have for about a year,
but then after that, you're just as happy
or unhappy as you were before you won
all the money. Well, because you spent
all the money by then. Perhaps, yeah. But it's interesting because
you sort of think that, you know, if only I could
just have a million dollars, I'll be set and, as it
turns out, it's fleeting. The interesting thing
is that we find that these exams that happen
every two to four years indicate that, over
the long term, whenever your friend
becomes happier increases your
own happiness. I mean, that's amazing. We have about two minutes
left in the show and I wanted to give
you a chance to talk about if you could control
the world in the future, taking some of
these principles, the PACE study that
you've been working on, the networking that
we're talking about, how would we impact schools,
public health? Where do you see
this going one day? Well, I think certainly
schools are a great place for us to have an impact
because they give us, first of all,
an educational opportunity and there have been
some unique programs already developed
for schools. We take the attitude that,
well, we can explain that you're overweight
and you have to make these changes and
you're going to do it. But if we try to do it
more from an educational point of view,
to explain why you should make healthy choices
and here are examples, and then let the schools
have the environment where they can make
a healthy choice, it's kind of silly for us
to talk about making healthy choices and
then they can go buy soda or they could buy
Flaming Hot Cheetos from the vending machines
to do that. If we're going to effect
the change in the house, this is a great place
to making a change because, if the child comes
home and says, oh, you know, I really like getting apples, I don't want to eat
the Fritos that you're giving me
all the time, potato chips, then maybe we can
affect a change within the house as well. So understanding
and I think certainly the study you were
just talking about with the smokers quitting in
a cluster is very encouraging because it does give
weight to the evidence that we need to maybe think
about these networks and attack a network
as opposed to just looking at an
individual to do that. We see that all the time,
again, in children. We can't just say
to a family where everybody in the family is obese
and we're just talking about the eight-year-old child
and say you have to make a change
and the other family members are allowed to continue
to do whatever they were doing before,
you'll have no success at all. Well, that's neat. This is exciting and
I'm so glad both of you could come join us
to talk about this because it's of
interest anyway, but it has impact
on peoples' lives and health. Whether you know it or not,
you've already impacted people and changed their health
as a political scientist. That's what doctors do, okay? That's what M.D. doctors do,
not the PhD doctors do. I mean, congratulations
on an incredible study and I know that you're
going to be continuing to work on this and I think
that's just spectacular. And thank you for coming
to talk to us about how important all this
is and how meaningful it is. – Thank you.
– Thank you. I appreciate you both
taking the time with us. You just heard
an incredible discussion about the impact
that your social network which includes your friends,
but for kids, their family network,
what that can have on your life and health. And the trick isn't
to get rid of your friends that have it, like,
if they're obese. Because that doesn't work,
we know that. But remember that
you do have influence and that you can change
and that actually can help the people
around you as well. So let's take advantage of
these networks and flip them. Knowledge is power. The more you know,
the more you can affect your own health and,
as it turns out, the health of your friends
and your family. I'm Dr. David Granet. This has been Health Matters. We'll see you again next time.


text:
For older people with hearing loss, the hearing aid selection can be confusing and painful, especially when they decide to shop online without the help of an ENT/dispenser/audiologist.
As a purchaser, when you are choosing a hearing aid model from a variety of suppliers, are you also confused? Today's article will try to explain several methods on choosing hearing aid models.
Based on your purchase budget
The most expensive component of the hearing aid is the amplifier/DSP (digital signal processor), so we can say that the budget basically limits and thus determines the amplifier/DSP.
If the purchase budget is below 20$, basically only analog hearing aids can meet the target.
For digital hearing aids, the most important thing is to choose the channel of the DSP, followed by the microphone and the receiver. Take Intricon's chips as an example, they have 2/4/6/8/16-channel chips. The higher the channel, more expensive procurement cost, the higher the manufacturer's factory price.
Of course, more advanced chips have more powerful functions. For example, only 4 channels or advanced more can be compatible with the Bluetooth module. 6 channels DSP has adaptive directionality, and 8 channels DSP have data logging.
Based on wear type
Traditional Behind-the-Ear Hearing Aid
Wearing behind the ear, the amplified sound is transmitted like this: the hearing aid amplifies the sound —> sound reaches the ear hook —> the thick tube connected to the ear hook transmits the sound to the user's ear canal.
This is the traditional design on the market. The advantage is that it is more suitable for users with severe hearing loss.
Open-fit Behind-the-Ear Hearing Aid
When the user wears the traditional BTE, it may cause the Occlusion effect, which promotes the birth of open fit design.
In addition to reducing the blocking effect, the open fit hearing aid is light in weight and more aesthetically pleasing than the thick tube.
In-the-Ear Hearing Aid (ITE)
Another major category is the ear canal hearing aid, and the specific subdivision includes ITC, CIC. Compared with BTE, ITE does not require a tube, and it can be directly worn with ear dome.
⇒ For purchaser, you need to know that the return rate of ITE may be higher than BTE. This is the conclusion we get from major customer's return rates. On the one hand, each person's ear canal is unique, so it's more likely that users feel ITE doesn't fit and then return; On the other hand, when the user pushes the ITE into the ear canal, usually the hearing aid has already started working so there will be squeal sound. For users who did not wear the hearing aid before, they will mistakenly think that this is howling and believe the product is faulty and returned.
Based on feature
*** with Rechargeability
Hearing aids use zinc-air batteries for a long time, and many distributors will provide users with a free battery for one year. With rechargeable hearing aids, there is no need that users bring zinc-air batteries.
Since Phonak launched its first rechargeable hearing aid, hearing aid manufactures are constantly developing the charging technology for hearing aids. Nowadays you easily find reachargeable aids everywhere.
*** with Telecoil
Telecoil is an option for many modern hearing aids. Telecoil is a small sensor or copper wire placed in a hearing aid. When activated, it wirelessly picks up magnetic signals from hearing-compatible systems (such as conference rooms, concert halls, museums, and even those in subways) and converts that signal into sound.
This type of technology helps people hear by eliminating most background noise and reverberation.
*** with Directional Microphone
Many modern hearing aids are equipped with a directional microphone. This technique works best when you are close to the sound source. Almost all hearing aids with this function can automatically switch between direction and omnidirectional settings depending on the environment.
*** with Feedback Suppression
Feedback suppression or digital feedback suppression helps eliminate high-pitched squeal.
*** Digital Noise Reduction (DNR)
By blocking some background noise, it makes listening and understanding speech easier.
*** with different Programs/Memory
People are social animals. We are always in different social life and environment. That's why we need different programs to meet each circumstance.
For example, you may have one program for quiet environments, one for noisy environments, and one for using the telephone. You could adjust the hearing aid on your own by pressing a memory button on the hearing aid or remote control.
Most hearing aids have two or three memories.
Based on different hearing loss level
You could choose different models based on customer's hearing loss level and match with the gain/output of hearing aids.
Based on your sales channel
If you offer hearing aids to customers face-to-face, programmable hearing aids will be great.
If it is online sales, you can choose hearing aids with preset programs to reduce programming troubles. For BTE think/thin tube, according to our past experience, users prefer open fit design, so try not to choose big ear hooks. Another better choice is the hearing aid with thin tube and ear hooks interchangeable. In general, the gain of the ear hook will be 5 dB higher than with the tube.
In addition, after-sales is crucial for online sales. For online sales purchaser, choose a supplier with good quality products and after-sales service eliminates your profits be consumed by returns. In the long run, although your purchasing costs go up, profits should be higher than buying cheap junky products.
Last words
Choosing hearing aid models is not an easy job, you need to consider all factors and make the best choice. We understand that you have your own set of procurement standards, but we wish to share with you more inside info to help with your purchasing. Contact AZ Hearing, we'd love to get your feedback.
- https://www.hearingaidknow.com/rechargeable-hearing-aids
- https://www.intricon.com/products/hearing-health/
- https://www.hearingchoices.com.au/hearing-aids-buyers-guide/
- https://www.consumerreports.org/cro/hearing-aids/buying-guide/index.htm
- https://www.everydayhearing.com/hearing-aids/articles/the-ultimate-guide-buying-hearing-aids/
Supplementary statement:
1. Some of the images in this article are from the Internet. If you infringe, please contact us and we will delete them as soon as possible.
2. This article contains some author's subjective view, we welcome reader's any feedback or question.


text:
Our New Look!!!………….. Where are we going from here??
With 35 Years behind us, I have reflected over the many steps of change that have brought us to the edge of retirement. This is a journey and there have been many bends in the road along the way.
When I first started I visited a consulting firm in Edmonton. After many hours of brainstorming I reluctantly removed "Mon-Gee" from my business name, a name that meant a lot to me. "Mon" was used because it represented my father's surname and "Gee" for Geraldine. However it did not have 'sales' appeal. We developed a new marketing plan and expanded the business into a spa. Then came the big change. A computer program would make business more efficient so I embarked on the technology world.
When I first started Pat Welter of Masterhand Designs was launching his career and made me my first sign to set up at #26 Brentwood Trailer Court.
In 2000 when I purchased the police barracks, Pat developed the beautiful blue sign that adorned the front lawn for 15 years. We ventured into new colors at the spa so a great way to start off the new look was a beautiful new sign created by Pat! Pat worked hard and brought color and meaning to the amazing sign that was ready for our 35th Anniversary on August 20th. Paul Marshal; a welder and great friend of Pat's, said to me that the Spa's new sign is some of Pat's best work. We are so proud of it!
We added butterflies and flowers to the spa trademark and chose lavender and pink to bring a calming effect to the ambiance. Kait shared her talent of colors and decor, giving birth to a total new look. We transferred this new vibe of colors and images through-out the treatment rooms in the spa and onto our business cards and brochures.
The Butterfly is the symbol of transformation. A caterpillar spins itself a cocoon and emerges as a beautiful butterfly. This is the feeling we want our clients to have when they leave the spa. We want them to feel new and fresh, with renewed balance and beauty. We want them to feel transformed and invigorated.
I will share the history of the colours that Pat so meticulously shared as he designed the sign. It compliments the healing that colors bring us. The study of color therapy is fascinating.
White represents all colors to create balance and harmony. The Blue is a cooling color and helps relieve inflammation, headaches, and high blood pressure. Brown represents the earth so helps with body stability and grounding. Magenta regulates the adrenaline and heart activity. Violet/Purple stimulates the spleen & white blood cells to increase your immunity & relieve emotional stress. Indigo purifies the blood stream. Yellow strengthens the nerves, stomach, liver, and intestines. It also speeds up the digestion. Orange increases the thyroid, stimulates the lungs, the digestive system and relieves muscle cramps & spasms.
To complete the image Pat has brought new life to our display boards for trade shows and Christmas craft fairs. Our new vertical banner will give a great visual to all who walk by. It will give a lasting impression.
Thank you Pat for your talent here in Unity. Thank you to Kait for sharing your visionary talent.
We will continue to serve you royally with our bountiful spa menu. Be sure to check it out and try something new.
Kneippe Therapy carries the bath oils using the colors derived from plants.
European Body Wraps are great and have amazing health benefits.
Jade Stone Hot and Cold Massage is indescribable and very relaxing.
Customized Eminence Organic Facials are absolutely memorable and rejuvenating. Kait does an excellent job.
Pedicures will make your feet happy and ready to dance through the autumn leaves.
Knieppe Therapy carries the bath oils using the colors derived from plants.
Check out Our Spa and Our Wonderfully Refreshing New Look! Our shelves are brimming with new Christmas lines for your shopping convenience right here in Unity.
Plan to take time to reflect in the solarium and come out rejuvenated. A solarium is a great place to journal and reflect on your day your week or your month. A way to add value to your life and achieve your dreams.
Geraldine Barrett


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