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Osteoarthritis is a joint disease with a complex etiology. It results in loss of normal joint function due to breakdown of articular cartilage. A consensus definition comes from a workshop held in 1995:
Approximately 37 million people in the United States suffer from some form of arthritis. In 1994 the Centers for Disease Control reported that by year 2020, when one out of every two Americans will be over the age of 50, there will be a larger increase in new cases of arthritis than of any other disease in the United States. Arthritis is at the top of the list of the leading causes of disability. Osteoarthritis its most common form and has the greatest economic impact. Because osteoarthritis is much more prevalent than rheumatoid arthritis (RA), the economic impact of osteoarthritis may be 30 times greater than that of RA. Osteoarthritis will soon account for more than 30% of office visits. As physicians, our most important contribution will be to limit days lost from work as well as the social and psychological impact of this devastating disease.
Osteoarthritis is primarily a disease of the articular cartilage. However, when damaged, other tissues (such as subchondral bones, synovia, ligaments and supporting neuromuscular apparatuses) will contribute to the acceleration of cartilage degradation. The components of articular cartilage include type II and other collagens, proteoglycans and chondrocytes. Nutrition of chondrocytes is provided by diffusion from the blood supply of subchondral bone and synovial fluid.
Types III, IV, IX, X and XI collagen make up 10 to 20% of the total cartilage collagen and maintain the stability of Type II collagen. For example, type IX and XI collagen regulate its fibril diameter. The proteoglycan aggrecan is highly hydrophilic, with low viscosity. Its ability to retain water under conditions of load and release it during unloading imparts to articular cartilage its elastic property, allowing the cartilage to function as a shock absorber in the diarthrodial joint. An abnormality in the structure of these proteins leads to cartilage with poor function and thus to the development of osteoarthritis.
Interleukin 1 (IL-1), a cytokine produced by mononuclear cells, synovial lining cells and chondrocytes, stimulates the chondrocyte to produce neutral metalloproteinases (collagenase, stromelysin and gelatinase) which degrade cartilage.[2] Other cytokines stimulate the chondrocyte to secrete tissue inhibitor of metalloproteinase (TIMP). Synthesis of cartilage components depends on growth factors such as insulin-like growth factor 1 (IGF-1) and transforming growth factor ß (TGFß).
Chondrocytes obtained from patients with osteoarthritis produce nitric oxide (NO), prostaglandins, tumor necrosis factor (TNF), IL-6 and IL. Since chondrocytes live in a milieu that is avascular and aneural, these mediators may not produce the classical signs of inflammation, but nevertheless they are involved in degradation of cartilate.[3]
With advancing age, the homeostatic mechanism that maintains the joint, fails. Cells are no longer able to maintain matrix and collagen production, and osteoarthritis develops. What initiates the shift in balance between degradation and repair of cartilage is not known. Trauma causing a microfracture or inflammation causing a slight increase in enzymatic activity may allow the formation of "wear" particles, which are then engulfed by resident macrophages. At some point in time, the production of these "wear" particles overwhelms the ability of the system to eliminate them and they become mediators of inflammation, stimulating the chondrocyte to release degradative enzymes. Molecules from breakdown of collagen and proteoglycan, also taken up by synovial macrophages, cause release of proinflammatory cytokines.[4] Both IL-1 and TNF increase prostaglandin synthesis by synovial cells, leading to further inflammation.
The effects of eicosanoid over-production, although initially thought to be on detrimental to cartilage metabolism, are now reported in experimental models to reveal a variety of both catabolic and anabolic activities depending on the end products produced (e.g. PGE1 or PGE2) and their interaction with different receptors and signaling pathways. The role of the lipoxygenase pathway in OA is still similarly unclear. Leukotriene B4 (LTB4) as well as leukotriene C4 production was found to be elevated in synovial fluid but not in chondrocytes in OA patients. LTB4 can also induce IL-1B production in synovial cells. The significance of these findings in terms of OA pathogenesis is still uncertain and merits further investigation.[5],[6]
Synovial inflammation (synovitis) is thought to be associated with structural damage and recent evidence links a number of biologic markers with high disease progression and structural damage[7] using molecular markers to monitor osteoarthritis. Elevated levels of cartilage oligomeric protein (COMP), a component of the extracellular matrix of articular cartilage formed by activated synovial cells, correlates possibly with active synovitis. Similarly, some evidence suggests that elevated levels of CRP (c-reactive protein) are predictive of long term radiological damage in knee OA[8] Levels of hyaluronic acid (HA) rise during inflammation.[9]
Expression factors for the proinflammatory gene nuclear factor kb (NF-kb) occur in osteoarthritic synovium, and nitric oxide (NO) is produced in synovial fluid from osteoarthritic joints. NO compromises chondrocyte survival,[10] affects IL-1 induced suppression of glycosaminoglycan and collagen synthesis, mediates IL-1 expression of matrix metalloproteinases and blocks production of IL-1 receptor antagonist (IL-1ra, a natural inhibitor of IL-1). Inhibitors of nitric oxide synthetase diminish arthritis in an animal model. Treatments that block NO or NO synthetase may treat osteoarthritis in the future.
Like other cells in the body "apoptosis" or programmed cell death plays a role in the disease process. Excess production of NO in OA tissues has be demonstrated to cause apoptosis of chondrocytes in vivo and invitro[11]. In addition, another mechanism contributing to chondrocyte apoptosis involves the expression of Fas antigen in a subpopulation of chondrocytes located in the superficial zone of cartilage. For apoptosis to occur these cells would have to come in contact with cells expressing Fas ligand (possibly inflammatory synovial cells).[12]
Osteoarthritis has several risk factors associated with its development, of which age is the greatest.[13]
A rare but exciting risk factor is a point mutation in the gene for type II procollagen in young patients with chondrodysplasia and precocious osteoarthritis, indicating that a genetic defect in assembly of matrix articular collagen is responsible for precocious osteoarthritis. A different point mutation occurs in patients with spondyloepiphyseal dysplasia who also develop premature osteoarthritis.
Epidemiological data suggest a genetic component to idiopathic osteoarthritis. Heberden's nodes (see Figure 8) are autosomally dominantly inherited in women and are associated with primary generalized osteoarthritis, a variant that involves multiple weight bearing joints in patients under the age of 50. In men Heberden's nodes are autosomally recessive. There may be an hormonal component to osteoarthritis, since estrogen replacement therapy confers a protective effect on its development in post-menopausal women.
Trauma is a risk factor for secondary osteoarthritis, especially periarticular injuries of the menisci, cruciate, and collateral ligaments of the knee, as well as fractures that involve the joint. Occupational injuries are less well established as risk factors, but studies report an increased incidence of osteoarthritis among jackhammer operators (wrists, hands and elbows), coal miners (knee), floor layers, construction workers, forestry workers and farmers, cotton pickers (fingers), and farmers (hips).[14],[15],[16] More recently, three more studies have related occupation to hip osteoarthritis.[17],[18],[19] Though a recent report noted an increased incidence of radiological but asymptomatic osteoarthritis in ex-female athletes and in a subgroup of control women engaged in long-term weight-bearing exercise, recreational sports are not associated with osteoarthritis in any age group.[20] Varus-valgus laxity, possibly related to defects in proprioception, may increase the risk of preventable knee osteoarthritis in women.[21]
The role of quadriceps strengthening exercises on already involved knees was further investigated by Sharma, L et al.[22] Adults with primary knee osteoarthritis were studied prospectively for eighteen months. Baseline quadriceps strength was measured and greater strength was associated with greater risk for progressive tibiofemoral joint space narrowing among adults with malaligned or very lax knees. Although these results do not imply that physical activity in adults with knee osteoarthritis is harmful it does call into question whether maximum quadriceps exercise in patients with malaligned and/or lax knees is protective or actually harmful.
Obesity is associated with preventable osteoarthritis of the knee in women.[23]
Lack of vitamin D predisposes patients with established osteoarthritis of the knee to further progression, and low levels of 25-OH Vitamin D are associated with radiographic progression of hip osteoarthritis.
Most clinicians divide osteoarthritis into two basic forms. Primary or idiopathic osteoarthritis refers to the type that occurs without any underlying predisposing factor. Secondary osteoarthritis follows an identifiable predisposing factor, either local or systemic.
Fewer patients have symptomatic disease than is seen on X-ray.
More than 80% of persons over the age of 50 have some radiographic evidence of osteoarthritis. The joints most commonly involved are the distal and proximal interphalangeals of the hand, first carpometacarpal of the wrist, hip, knee and cervical and lumbar spine, in an asymmetrical fashion.
Pain is the most prominent feature and the most common presenting complaint of osteoarthritis. Pain appears upon motion of the affected joint and resolves with rest. Since cartilage has no nerve supply, the pain comes from subchondral bone, synovium, joint capsule, ligaments, and muscle. Passive and active motion of the joint elicits pain, and coarse crepitus on motion may be heard or palpated. Although the sources of pain are well known, the perception of pain depends on the relationship between structural change and peripheral and central pain processing, with input from cultural, gender, and psychological factors.[24] Since the major symptom of osteoarthritis is pain, consideration of all of these issues is important in the treatment plan.
In osteoarthritis, stiffness in the morning typically lasts less than 20 minutes. After being immobile, some patients report a transient stiffness, the so-called "gelling phenomenon," which also lasts no longer than 20 minutes. In contrast, in rheumatoid arthritis, gelling lasts for several hours. Osteoarthritis is not associated with the presence of fever, weight loss, anorexia, severe muscle atrophy, or symmetry of joint involvement.
As the disease progresses decreased range of motion occurs because of joint surface incongruity and because of increased pain with motion. Other reasons for decreased range of motion are muscle spasm and contracture, capsular contracture, and mechanical problems related to osteophytes or loose bodies in the joint. Accumulation of synovial fluid may contribute to pain, decreased range of motion, and distention of the capsule.
Advanced disease is associated with subluxation of the joint and gross deformity. In osteoarthritis, Heberden's nodes are bony enlargements of the distal interphalangeal joints with loss of joint space and osteophyte formation. Small gelatinous cysts (synovial herniations) may also be seen alongside the node. A similar bony enlargement of the proximal interphalangeal joints is called a Bouchard's node.
Heberden's and Bouchard's nodes begin after age 45 and affect women more than men by 10:1. Heredity plays an important role in their development in women. Most are asymptomatic but some at onset are inflamed and painful. Involvement of the first carpometacarpal joint (base of the thumb) limits a patient's ability to open jars or use the wrist. Symptoms in this joint are the only evidence of wrist involvement in osteoarthritis and clearly differentiate it from rheumatoid arthritis, in which the entire wrist is swollen. Often the joint will sublux and give the hand a "squared off" appearance.
The talonavicular and the first metatarsophalangeal joints are the most common joints involved in the feet. In the metatarsophalangeal joint, bunion formation causes pain and widening of the foot. In addition hallux rigidus (rigid great toe) can also occur, limiting motion and causing difficulty in walking. Very often the patient finds he must buy wider shoes to accommodate the deformity.
A rocker bar placed under the first metatarsophalangeal joint is often very effective in decreasing pain. Pain on inversion and eversion motions of the ankle is usually due to degenerative osteoarthritis of the subtalar or talonavicular joint and should be differentiated from the true ankle joint (tibiotalar, plantar and dorsiflexion of the foot) arthritis, which is more likely to be due to traumatic secondary osteoarthritis.
Hip osteoarthritis is more common in men, is usually unilateral, and causes a characteristic painful (antalgic) gait. Very often, hip pain is referred to the knee. In hip disease, the following motions are impaired, in order of frequency: internal rotation in flexion, internal rotation in extension, flexion, external rotation in flexion, external rotation in extension, and extension.
Knee osteoarthritis is common. Unlike rheumatoid arthritis, osteoarthritis is of usually limited to a single (patellofemoral, medial, or lateral) compartment of the knee and is not symmetrical. The effusions are less inflammatory in osteoarthritis than in rheumatoid arthritis. Loss of lateral compartment joint space causes genu valgus or "knock knee". Loss of medial compartment space leads to genu varus or a "bow legs". In patellofemoral involvement the patient complains of anterior pain usually going up (more than down) stairs.
The laboratory evaluation in osteoarthritis is important for the lack of positive findings associated with the disease. Routine tests such as blood count, urinalysis, sedimentation rate (also known as erythrocyte sedimentation rate or ESR), biochemistries, and specialized tests such as rheumatoid factor, antinuclear antibody, and thyroid function tests are normal but useful to exclude other disease. However, the elderly have a high incidence of rheumatoid factor, antinuclear antibody, and elevated ESR without obvious illness. The history and clinical presentation are the most important elements of diagnosing a specific type of arthritis. The laboratory helps support, rule out, or subclassify a clinical diagnosis.
Synovial fluid analysis should be done on joints with large effusions. In osteoarthritis aspiration should demonstrate clear fluid with a cell count of less than 10,000 WBC/mm3 (higher than this suggests inflammatory arthritis or infection) with normal protein and glucose, good viscosity, and a negative polarized light microscopic examination for crystals. (When aspirating any joint, use aseptic technique, wear gloves, and send a specimen from every aspiration of joint fluid for culture and sensitivity regardless of the working diagnosis.)
Measurement of degradation components of cartilage of cartilage and matrix in serum, urine or joint fluid has attracted much recent interest, since finding evidence of early cartilage breakdown might lead to earlier diagnosis and intervention. One can measure constituents of the extracellular matrix, (proteoglycans [aggrecan], collagen, and non-collagenous proteins), degradative proteolytic enzymes, cytokines, and nitric oxide. Measurement of these products in joint fluid offers an advantage in that the concentration will be higher and demonstration of their presence more specific than in serum. However, assessment of biologic markers is still experimental.[25],[26]
X-ray evaluation is the "gold standard" in the diagnosis of osteoarthritis.
X-rays of the knee and hip should always be obtained weight bearing. For the knee, it is helpful to obtain a lateral and Merchant view to evaluate the patellofemoral joint. In addition one should do a standing semi-flexed view of the knee to approximate the normal anatomic standing position (Buckland-Wright)
Joint space narrowing is a non-specific finding that results from degeneration and disappearance of the articular cartilage for any cause. Increased bone density due to subchondral bony sclerosis and marginal osteophyte formation is more specific for osteoarthritis. Osteophytes are a late sign. Bone cysts are seen as periarticular translucent areas. Bone scans may be useful to rule out fracture due to metabolic, traumatic, or metastatic causes; mild increased activity at the involved joints is commonly seen in osteoarthritis. Bone scan coupled with radio-labeled bone-seeking diphosphonates may predict subsequent radiographic progression. Nuclear magnetic resonance imaging (MRI) is extremely helpful in the spine and has almost replaced computerized tomography (CT) scanning and myelography in defining disc disease, tumors, and spinal stenosis.
X-ray changes in osteoarthritis occur slowly and the possible value of MRI in the future would be in allowing investigators to demonstrate a change in the progression of the disease with medication in a shorter period of time. Methodologies are now being developed and validated to look at surrogate markers such as Global Cartilage Volume loss. Correlations with X-ray joint space narrowing in patients with osteoarthritis are being defined and related to fast and slow progressors. In preliminary data by Jean-Pierre Pelletier, it appears as if medial meniscal extrusion (but a not a simple tear of the medial meniscus) is associated with significant cartilage volume loss at 2 years.
MRI otherwise offers little benefit in the evaluation of primary osteoarthritis but may also be helpful in identifying avascular necrosis, pigmented villonodular synovitis, and internal derangement of the knee. In sports injuries MRI changes correlate with changes seen at arthroscopy.
The key to differentiating among the various rheumatic diseases is first to divide the diseases into inflammatory and non-inflammatory categories. Patients in the former category have swelling and systemic symptoms, such as morning stiffness and fatigue, and may have extraarticular features such as olecranon nodules. Next, determine whether the illness is symmetric or asymmetric, and whether its onset is gradual or acute. Lastly, define its course as progressive or episodic, with flares and remissions. Osteoarthritis is asymmetric, unassociated with extraarticular or systemic features, and has a gradual onset. Careful correlation of the clinical, laboratory and X-ray findings is important.
Rheumatoid arthritis is the illness that many clinicians confuse with osteoarthritis. Rheumatoid factor is not diagnostic of rheumatoid arthritis. In contrast to the inflammatory conditions (polymyalgia rheumatica, rheumatoid arthritis, psoriatic arthritis, etc.), anemia is not a feature of osteoarthritis. In rheumatoid arthritis a symmetrical pattern of joint involvement is almost always seen, while osteoarthritis is usually a disease of asymmetry affecting the large joints and spine. Osteoarthritis affects the first carpometacarpal joint but rarely (unless secondary to trauma) the other joints of the wrists, while rheumatoid arthritis affects the wrists in a symmetrical fashion. In osteoarthritis the distal interphalangeal joints are involved in an asymmetric manner, whereas in rheumatoid arthritis these joints are spared and the metacarpophalangeal joints are symmetrically involved. Although in osteoarthritis any one hand joint may become inflamed and show and erosion (erosive osteoarthritis), in rheumatoid arthritis most joints become eroded in a more or less symmetric fashion. Occasionally rheumatoid and osteoarthritis coexist. (Any joint that is damaged by one form of arthritis may eventually develop secondary osteoarthritis.) The X-ray features are quite distinct, with rheumatoid arthritis having osteopenia and erosive disease in contradistinction to osteoarthritis in which osteophytes and subchondral sclerosis occur.
In examining the hip, it is important to determine whether motion of the hip causes the patient's pain, particularly pain referred to the knee. To differentiate hip pain from lumbosacral radicular pain, note that hip pain does not radiate below the knee into the calf, but radicular pain does. If the source is lumbosacral-radicular, active motion of the hip in flexion does not reproduce the patient's pain. Because both sources of pain can exist simultaneously it is important to determine which is the predominant complaint. A careful neurologic exam combined with electromyography will be of some help. Although some physicians inject the hip with lidocaine to determine the origin of pain, I have found this technique to be of little help.
Another cause of pain about the hip is trochanteric bursitis. This patient complains of lateral hip pain, but has good (gentle) passive range of motion. In contrast to pain truly originating from the hip, tenderness is localized over the greater trochanter on the lateral aspect of the leg and not in the groin. In this case injecting the bursa with lidocaine and corticosteroid often gives excellent relief.
Before starting therapy, the physician must do a complete evaluation, including a medication history, medical history, and physical exam. Many patients with osteoarthritis are elderly, have co-morbid medical conditions, and take medications that may interact with those prescribed for osteoarthritis. In addition, when the physician does a complete evaluation, other conditions (such as cancer or thyroid disease) that may cause joint pain can be identified and treated properly.
Treatment is aimed at control of pain by decreasing inflammation in the joint, adjuvant control with analgesics, and physical and occupational therapy modalities.[27]
All too often, patients who receive a diagnosis of arthritis envision themselves in a wheelchair. The physician's first duty after diagnosis is education. A straightforward discussion of prognosis is always helpful, and the patient should encourage the physician to provide it. Disease-specific pamphlets, are available from the local chapter of the Arthritis Foundation. A list of pamphlets can also be obtained from the headquarters of the Arthritis Foundation, located in Atlanta, by calling 1-800-283-7800.
The American College of Rheumatology Guidelines for the Diagnosis and Treatment of Osteoarthritis of the Hip and Knee suggests that drug therapy should begin with simple analgesics such as acetaminophen.[30] These guidelines were derived from data which demonstrated that the first available non-steroidal anti-inflammatory drugs (NSAIDs), which are non-specific cyclooxygenase inhibitors, were costly in terms of side effects (gastric ulcerations, perforations and hemorrhages) and had no higher benefit than that afforded by acetaminophen. The discovery and release of cyclooxygenase-2 (COX-2) specific NSAIDs, with their superior safety profiles, allows clinicians to return to the use of anti-inflammatory medication as the first step in drug management of osteoarthritis.
Professor John Vane won the Nobel Prize for elucidating the mechanism of action of aspirin. It, and other NSAIDs, block the enzyme cyclooxygenase, which converts arachidonic acid to prostaglandin. Prostaglandins are short-lived substances that act as local hormones (autocoids), of which prostaglandin E2 is the principal one active in inflammation. NSAIDs represent the most widely prescribed class of drugs in the world and are second only to antihypertensives in being prescribed for long periods of time in any one patient. Side effects involving the gastrointestinal, renal and hematopoietic systems have limited their usefulness.
A second cyclooxygenase enzyme (COX-2) system has been described. Inhibition of COX-2 confers anti-inflammatory effects without inhibiting the (COX-1 generated) prostaglandins that are important for normal function of the stomach and platelets. Celecoxib (Celebrex) 200mg/day, and rofecoxib (Vioxx) 12.5-25mg/day (Vioxx was voluntarily withdrawn by Merck from the market as of 9/30/04-see next paragraph), represent the first generation of specific COX-2 inhibitors approved for the treatment of osteoarthritis, followed by Valdecoxib (Bextra), a second generation COX-2. Two large studies recently attempted to document superior gastrointestinal safety of the COX-2 agents, but fell short of proving the point without a doubt because of methodological problems.[31],[32] However, most physicians, based on these results, coupled with several prelaunch safety and efficacy studies with these agents, believe in their GI safety.
The incidence of stroke, myocardial infarction, edema, hypertension and gastrointestinal events with or without concomitant use of aspirin have been under continuous review by the FDA since the launch of the COX-2 inhibitors. Merck, Inc., on 9/30/04, voluntarily withdrew Vioxx from the marketplace. Their decision was based on a recent double blind 3 year study (APPROVe trial) of 2600 patients who were treated with 25mg of Vioxx to prevent colonic polyps. In this cohort, after 18 months of taking the medication there were close to 50% more cardiovascular events(stroke and myocardial infarct) than in the placebo group. In actuality there were 25 confirmed cardiovascular events in 3351 patient years of exposure on placebo(0.75events per 100 patient years) and 45 cardiovascular events in 3041 patients years of exposure on Vioxx(1.48 events per 100 patient years). This represents a relative risk of 1.98 with 95%CI (1.201-3.192) (p=0.0071). In a further subgroup analysis the relative risk was the same whether or not the patients took concomitant aspirin. Mortality was similar and low -- 5 death with Vioxx and 5 taking placebo. Although the number of patients involved was small compared to those treated (approx 70 out of 2600) and occurred after 18 months of treatment, the company still felt obligated to withdraw the drug from the market (a responsible act based on the data). Since the numbers are small, what impact this may for have on any individual patient taking Vioxx is unknown but probably small. Vioxx has a different chemical structure and metabolic breakdown products than the other COX-2 inhibitors on the market. These are valdecoxib (Bextra), celecoxib (Celebrex) and the COX-2 selective meloxicam (Mobic). As such, the increase in cardiovascular events should not be interpreted as a "class effect" of COX-2 inhibitors. Meloxicam, valdecoxib and celcoxib have not been demonstrated in any clinical trials to have an increased incidence of stroke or myocardial infarct. A recently published safety trial of lumiracoxib (Prexige), another COX-2 inhibitor in development, likewise failed to demonstrate any increase in stroke or myocardial infarct (Farkouh,M.E. et al Lancet 364675-683,2004).
Two recent publications from observational data bases in the Canadian health care system comprising over 1.5 million patients over the age of 65 demonstrated the improved GI safety of Vioxx and Celebrex over non selective NSAIDS.[33],[34] The real question of whether a cox-2 inhibitor plus low-dose aspirin (in those who need to take aspirin for cardiovascular protection) is safer than traditional NSAIDs and low-dose aspirin has only been approached but not fully answered. A meta-analysis of short trials of celecoxib by Deeks et al[35] demonstrated that the GI safety of celecoxib plus low-dose aspirin was less than celecoxicib alone but much safer than traditional NSAID plus celecoxicib. A recent state of the art report by Fitzgerald et al address the relevance of this question and gives us some guidelines to follow. A COX-2 inhibitor in development (lumiracoxib) will present data from an >18,000 prospectively studied safety database that will hopefully shed more light on this important issue.
Meloxicam (Mobic) is a newer non-steroidal anti-inflammatory agent with a safety profile documented to be similar to that of the specific COX-2 inhibitors. Initial drug therapy of osteoarthritis with NSAIDs is now again possible. However, not all patients benefit from these drugs and some develop side effects, including nausea, diarrhea, and edema. COX-2 inhibitors do not affect platelet function and may, carefully, be used in anticoagulated patients. Like non-selective inhibitors, selective COX-2 inhibitors may cause water retention (edema). Whether they also affect renal function in normal patients is still unknown.
If COX-2 inhibitors are ineffective or have to be discontinued because of side effects then therapy can begin with simple analgesics. In addition, analgesics are excellent adjuvant therapy for patients on NSAIDs who have breakthrough pain. NSAIDs will generally work in three weeks and need not be continued if ineffective. A well-controlled trial of diclofenac plus misoprostol versus acetaminophen in patients with osteoarthritis of the hip or knee by Pincus et al[36] - plus an accompanying editorial by Felson[37] - appears to once again validate the superiority of NSAIDS over simple analgesics in the treatment of osteoarthritis.
We recommend monitoring patients on NSAIDs with baseline then three to four-monthly CBC, platelet count, biochemistries, (liver function and renal tests) and urinalysis.
Corticosteroids, either parental or oral, have no role in the treatment of osteoarthritis. However, injection with intra-articular steroids for a particularly painful joint is, at times, helpful. Use aseptic technique, aspirate the joint and send some fluid for culture and sensitivity; then inject either methylprednisolone acetate 40 mg/ml or triamcinolone hexacetonide 20 mg/ml into the joint. These preparations should be combined with 1 cc of lidocaine in large joints such as the knee, shoulder, and ankle. For the wrist one uses one-half this amount, and for small joints of the hand one should use a tuberculin syringe with a mixture of 0.1 cc lidocaine and 0.1 cc of methylprednisolone acetate 40mg/ml. Do not inject any one joint more than four times per year. Each injection should result in at least three months of relief. Pain relief lasting less than 2-3 months should be considered a failure and not repeated.
Viscosupplementation, a therapy proven useful in animals, has been developed to treat patients with long standing painful osteoarthritis who might not be appropriate for traditional therapy. In normal joints synovial fluid changes from viscous to elastic with increasing load, providing a frictionless surface. Hyaluronic acid, a high molecular weight component of synovial fluid, is composed of N-acetyl glucosamine and glucuronic acid. Enzymes and free radicals generated during inflammation in osteoarthritis degrade hyaluronic acid causing it to lose its viscous and elastic properties. The degraded hyaluronic acid itself contributes to articular damage. Viscosupplementation with hyaluronic acid may delay and possibly halt progression of osteoarthritis. Two preparations have been approved for treatment of knee osteoarthritis. One preparation (Hyalgan®), isolated from rooster combs, requires five weekly injections while the other (Synvisc®), a higher molecular weight product, made by cross-linking hyaluronic molecules with formaldehyde and vinylsulfone, requires three weekly injections. There have been few clinical trials of good design with both products; nevertheless, both have demonstrated efficacy compared to either placebo injection with saline or treatment with NSAIDs[38],[39] A growing body of data in animal models suggests that injection of hyaluronic acid increases the level of endogenous hyaluronic acid, decreases degradation of cartilage proteoglycans, inhibits the release of arachidonate and inhibits prostaglandin E2 synthesis. Tidal lavage of an osteoarthritic joint with saline has not stood the clinical test of time. A new synthetic form of viscosupplementation offering one injection, with efficacy lasting up to six months, is now in phase III testing.
Since the publication of The Arthritis Cure and Maximizing the Arthritis Cure by Jason Theodosakis, MD, the use of nutritional supplements containing glucosamine and chondroitin sulfate has skyrocketed. Both publications claimed that these agents treat the symptoms of osteoarthritis and retard structural damage. Several European clinical trials suggested that these agents have effects in osteoarthritis similar to that of NSAIDs but have slower onset of action. Two recent meta-analyses concluded that, although the agents may show benefit, available studies provide insufficient information about study design and route of administration to allow definitive evaluation.[40] A recent publication reported on a three-year study in patients with osteoarthritis of the knee randomized to either glucosamine sulfate 1500 mg per day or placebo. After three years, the patients on glucosamine appeared not only to have clinical improvement, but there was also less progression seen in their radiographs. This represents the first well-controlled study on this subject. It did not, however, look at the addition of chondroitin sulfate, which has been touted to have synergistic properties when added to glucosamine.[41] The Office of Alternative Medicine of the National Institutes of Health has initiated a large placebo-controlled trial of glucosamine, chondroitin sulfate, and the combination of both. Pending completion of this trial, since these are nutritional supplements, they can be sold without approval by any governmental agency without safety standards. One only has to remember the epidemic of eosinophilic fasciitis that occurred with widespread use of L-tryptophan to understand the possible risk.
What should be the response of the physician faced with the question, Should I use glucosamine or chondroitin sulfate?" or "My aunt says this works for her?" I counsel my patients that I can and should inform them of therapies that have been scientifically proven and safe. In addition, I acknowledge their frustration and explain that we don't have all the answers. I recognize that in the treatment of arthritis anecdotes abound, but I feel strongly about recommending only products that I am convinced are safe and effective. Lastly, regardless of what the patient does, even if I don't condone it, I will still be available to treat him. I always stress that we look forward to scientific studies (such as the NIH one described above) that will answer the questions they have raised about an unproved remedy.
S-Adenosyl-L-Methionine (SAMe), advertised as effective for osteoarthritis, is a natural compound involved in sulfuration and methylation reactions. These reactions are important in both the generation of cytokines, which affect synovial cell function, as well as reactions involved in proteoglycan synthesis. Although some animal studies are encouraging in demonstrating improvement in cartilage histology, a few short-term clinical studies have not demonstrated any superiority over standard drug therapy. Although a "natural substance", SAMe is a regulator of homocysteine metabolism and possible effects on cardiovascular disease remains an unknown possibility.
Future: Experimental Therapies
Unlike rheumatoid arthritis, the development of agents that will not only decrease symptoms but also prevent further destruction (disease modifying anti-rheumatic drugs or DMARDs, also known as structural modifying antirheumatic drugs or SMARDS) for osteoarthritis has suffered from methodological problems - the least of which is the long time it takes for the disease to manifest itself. Nevertheless, several compounds are now being tested, e.g., risedronate (Actonel) in OA, The Guinea Pig Model. Use of Actonel in this model decreases chondrocyte loss and slows X-ray progression. This observation has been extended to clinical trials now in progress looking at the role of Actonel in preventing or stabilizing joint space narrowing in patients with moderate knee osteoarthritis.
The potential long-term treatment or cure of osteoarthritis lies in the development of agents that reverse the balance between degradative and synthetic processes of the chondrocyte. In animal studies doxycycline inhibits cartilage collagenase activity and reduces the severity of osteoarthritis. Transforming growth factor beta (TGFß), packaged in liposomes, can repair partial thickness articular cartilage lesions in animal models. Many pharmaceutical companies are testing pharmacological inhibitors of enzymes responsible for cartilage matrix destruction (metalloproteinases) and blockers of cytokines. Tetracyclines are inhibitors of tissue metalloproteinases (MMPs), possibly through their action on nitric oxide or via chelating the zinc present in the active site of MMPs. This function is separate from their antimicrobial activity. A national multi-center double blind randomized placebo-controlled trial looking at disease or structural modification in obese females with knee osteoarthritis is presently in progress.
Lay press reports of autologous chondrocyte transplantation for traumatic osteoarthritis has excited the public.[42] This procedure consists of removing cartilage cells from a non-weight-bearing portion of the knee via arthroscopy, growing the cells with growth factors in tissue culture, then transplanting them back into a defect under a periosteal patch. The investigators have had some success repairing weight-bearing cartilage defects of less than 3 cm. While this procedure may be applied to young individuals with traumatic injuries less than 3 cm., for whom the goal is to prevent secondary osteoarthritis, this procedure will not rejuvenate an end-stage osteoarthritic knee.
Gene therapy is another strategy in which non-replicating viral vectors can deliver genes that have either anti-arthritic or synthetic properties to the synovium and articular cartilage. Two human trials are presently underway in which a retrovirus transfers human IL-1ra cDNA to the synovial lining of metacarpophalangeal joints of patients with rheumatoid arthritis. In experimental osteoarthritis, IL-1ra transferred to the synovial lining of canine knee joints shortly after ACL transection reduced early cartilaginous lesions in the tibial plateau. However, the transfer by gene therapy of TGF-b and bone morphogenic protein 7 (BMP-7) to synovium and chrondroprogenitor cells resulted in death of some animals, possibly through overproduction of the proteins generated.
When conservative measures of treating osteoarthritis fail, and when pain in a specific joint disables an active individual, then targeted surgical intervention may restore a patient to normal activity. The general physician will be expected to counsel his patient about the proper procedure and to the proper timing of these interventions. A few guidelines follow. Surgery relieves pain more than it restores range of motion. Thus, the decision to operate is one more of personal than of medical priorities. The best candidate for surgery is the patient who has a definite interruption in some activity of daily living (can't walk more than a block, awakens from sleep with pain in the affected joint) and who has failed exercise and pharmacological therapy. For this patient the result will be outstanding because he will be pain-free in the involved joint.
In hip and knee osteoarthritis for patients over the age of fifty total joint replacement is the therapy of choice. The decision between cemented or non-cemented prosthesis is a technical one revolving around the age of the patient, the condition of the joint, and the surgeon's experience. Since total joint replacements have an average 15-20 year life before they risk of failure, young patients may need two or more revisions. With each revision the bone stock is less and the procedure more difficult. For this reason many surgeons suggest that younger patients undergo an osteotomy of the hip and knee before total joint arthroplasty. In this procedure the joint is realigned to distribute weight more evenly to the remaining articular cartilage. Although the recovery period is considerably more than that of total joint arthroplasty, this procedure generally relieves pain for up to five years and delays the need for a total joint replacement.
For the ankle, total joint replacement is not yet well perfected, but arthrodesis is a good procedure that limits pain by eliminating motion in the affected joint without great loss of mobility.
In the hand, distal interphalangeal involvement should not be surgically treated. If persistent mucous cysts are bothersome they can be excised. For the carpometacarpal joint of the thumb, implants have failed, but reconstruction interposing a part of the flexor carpi radialis tendon has shown remarkable results in relief of pain without loss of stability.
Total joint replacements are never stronger than the original joint. Post surgery, competitive sports are not usually possible, but golf, walking, and even doubles tennis are permissible. The risk of infection in the hands of an experienced orthopaedist should be less than 1% if the patient remains careful and treats the joint like a new heart valve. The total joint replacement patient should use prophylactic antibiotics for invasive procedures such as dental work, cystoscopy or colonoscopy. Guidelines issued in The Medical Letter, vol 41 (Issue 1060), August 27,1999, are as follows:
Antibiotic prophylaxis regimens for these kinds of invasive procedures:
Patients allergic to penicillin or amoxicillin should have one of the following regimens:
In my opinion, the physician should refer the patient to an orthopaedic surgeon who not only has specific training in joint arthroplasty, but who spends the majority of his time doing only these procedures. Specialists in joint arthroplasty should be associated with medical centers that have laminar flow operating rooms or similar infection control procedures.
The prognosis for patients with osteoarthritis is good, but definitely dependent on the joint involved and the occupation or physical needs of the patient. For example a patient with osteoarthritis of carpometacarpal joint of the thumb is not disabled unless he requires constant use of his hand. Disability due to advanced disease of the hip and knees in most cases easily responds to surgical therapy, but involvement of the spine that compresses nerves may cause neurologic damage that does not reverse after surgical relief. Patients with a large number of osteoarthritic joints tend to experience more rapid progression to knee osteoarthritis than do those with fewer joints involved, and those with bilateral knee osteoarthritis also have a fast rate of deterioration.
Although medication has not been proven to prevent progression of osteoarthritis, it controls pain and improves quality of life. New treatments are being tested to stop the progression of cartilage damage. Disability is uncommon, and outlook for those temporarily incapacitated is excellent with treatment.
The primary care physician, using the guidelines outlined, if quite careful when diagnosing osteoarthritis, need refer few patients. Referral to a rheumatologist will be helpful to:
A. Confirm a questionable diagnosis;
B. Sort out causes of secondary osteoarthritis and their potential treatments;
C. Initiate programs of proper physical therapy and joint protection;
D. Manage complex medication problems; and
E. Consult as to the type and place for surgery in the treatment plan. After evaluation, the rheumatologist ought refer the patient back to the primary care physician for management, with appropriate recommendations.
[1] Osteoarthritic Disorders: Workshop. Monterey, California, April 1995. Klaus E. Kuettner, Victor M. Goldberg, eds., American Academy of Orthopaedic Surgeons. June 1995.
[2] Woessner J Jr. The family of matrix metalloproteinases. Ann N Y Acad Sci. 1994 Sep 6;732:11-21.
[3] Attur MG, Patel IR, Patel RN, Abramson SB, Amin AR Autocrine production of IL-1 beta by human osteoarthritis-affected cartilage and differential regulation of endogenous nitric oxide, IL-6, prostaglandin E2, and IL-8. Proc Assoc Am Physicians. 1998 Jan-Feb;110(1):65-72.
[4] Thonar EJ, Shimmer M, Lohmander LS. Body fluid markers of cartilage changes in osteoarthritis. Rheum Dis Clin North Am. 1993 Aug;19(3):635-57.
[5] Wittenberg RH, et. al. In vitro release of prostaglandins and leukotrienes from synovial tissue, cartilage, and bone in degenerative joint diseases. Arthritis Rheum. 1993 Oct;36(10):1444-50.
[6] Abramson, SB. The role of COX-2 produced by cartilage in arthritis. Osteoarthritis Cartilage. 1999 Jul;7(4):380-1. Review.
[7] Otterness IG, Saltarelli MJ. Using molecular markers to monitor osteoarthritis. In Tsokos GC etc. editors Modern therapeutics in rheumatic disease, Totowa NJ Humana Press.
[8] Sharif M, Shepstone L, Elson CJ, Dieppe PA, Kirwan JR. Increased serum C reactive protein may reflect events that precede radiographic progression in osteoarthritis of the knee. Ann Rheum Dis. 2000 Jan;59(1):71-4.
[9] Goldberg, RL, Huff JP, Lenz ME, Glickman P, Katz R, Thonar EJ. Elevated plasma levels of hyaluronate in patients with osteoarthritis and rheumatoid arthritis. Arthritis Rheum. 1991 Jul;34(7):799-807.
[10] Blanco FJ, Ochs, RL, Schwarz H, Lotz M. Chondrocyte apoptosis induced by nitric oxide. Am J Pathol. 1995 Jan;146(1):75-85.
[11] Hashimoto S, Takahashi K, Amiel D, Coutts RD, Lotz M. Chondrocyte apoptosis and nitric oxide production during experimentally induced osteoarthritis. Arthritis Rheum. 1998 Jul;41(7):1266-74.
[12] Hashimoto S, Setareh M, Ochs RL, Lotz M. Fas/Fas ligand expression and induction of apoptosis in chondrocytes. Arthritis Rheum. 1997 Oct;40(10):1749-55.
[13] Felson DT, et al. Osteoarthritis: new insights. Part 1: the disease and its risk factors. Ann Intern Med. 2000 Oct 17;133(8):635-46.
[14] Hochberg MC, Lethbridge-Cejku M. Epidemiologic considerations in the primary prevention of osteoarthritis. In Hamerman D, ed. Osteoarthritis: Public Health Implications For An Aging Population. Baltimore: John Hopkins University Press 1997, pp 169-186.
[15] Jensen LK, Mikkelsin S, Loft IP, Eenberg W, Bergmann I, Logager V. Radiographic knee osteoarthritis in floorlayers and carpenters. Scand J Work Environ Health. 2000 Jun;26(3):257-62.
[16] Sandmark H, Hogstedt C. Vingard E. Primary osteoarthrosis of the knee in men and women as a result of lifelong physical load from work. Scand J Work Environ Health. 2000 Feb;26(1):20-5.
[17] Lau EC, Cooper C, Lam D, et al. Factors associated with osteoarthritis of the hip and knee in Hong Kong Chinese: obesity, joint injury, and occupational activities. Am J Epidemiol. 2000 Nov 1;152(9):855-62.
[18] Yoshimura N, Sasaki S, Iwasaki K, et al. Occupational lifting is associated with hip osteoarthritis: a Japanese case-control study. J Rheumatol. 2000 Feb;27(2):434-40.
[19] Vingard E, Alfredsson L, and Malchau H. Osteoarthrosis of the hip in women and its relation to physical load at work and in the home. Ann Rheum Dis. 1997 May;56(5):293-8
[20] Spector DT, Harris PA, Hart DJ, et al. Risk of osteoarthritis associated with long-term weight-bearing sports: a radiologic survey of the hips and knees in female ex-athletes and population controls. Arthritis Rheum. 1996 Jun;39(6):988-95.
[21] Sharma L, Song J, Felson DT, et al. The role of knee alignment in disease progression and functional decline in knee osteoarthritis. JAMA. 2001 Jul 11;286(2):188-95.
[22] Sharma L, Dunlop DD, Cahue S, Song J, Hayes KW. Quadriceps strength and osteoarthritis progression in malaligned and lax knees. Ann Intern Med. 2003 Apr 15;138(8):613-9.
[23] Felson DT, Zhang Y, Anthony JM, et al. Weight loss reduces the risk for symptomatic knee osteoarthritis in women. The Framingham Study. Ann Intern Med. 1992 Apr 1;116(7):535-9.
[24] Creamer P, Hochberg MC. Why does osteoarthritis of the knee hurt--sometimes? Br J Rheumatol. 1997 Jul;36(7):726-8.
[25] Wollheim FA. Serum markers of articular cartilage damage and repair. Rheum Dis Clin North Am. 1999 May;25(2):417-32, viii.
[26] Myers SL, Synovial fluid markers in osteoarthritis. Rheum Dis Clin North Am. 1999 May;25(2):433-49, viii-ix.
[27] Felson D, et al. Osteoarthritis: new insights. Part 2: treatment approaches. Ann Intern Med. 2000 Nov 7;133(9):726-37.
[28] Puett DW, Griffin MR. Published trials of nonmedicinal and noninvasive therapies for hip and knee osteoarthritis. Ann Intern Med. 1994 Jul 15;121(2):133-40.
[29] Kaptchuk, RJ. Acupuncture: theory, efficacy, and practice. Ann Intern Med. 2002 Mar 5;136(5):374-83.
[30] Recommendations for the medical management of osteoarthritis of the hip and knee: 200 update. American College of Rheumatology Subcommittee on Osteoarthritis Guidelines. Arthritis Rheum. 2000 Sep;43(9):1905-15.
[31] Silverstein F, Faich G, Goldstein JL, et al. Gastrointestinal toxicity with celecoxib vs nonsteroidal anti-inflammatory drugs for osteoarthritis and rheumatoid arthritis: the CLASS study: A randomized controlled trial. Celecoxib Long-term Arthritis Safety Study. JAMA. 2000 Sep 13;284(10):1247-55.
[32] Bombardier C, Laine L, Reicin A, Shapiro D, Burgos-Vargas R, Davis B, Day R, Ferraz MB, Hawkey CJ, Hochberg MC, Kvien TK, Schnitzer TJ. Comparison of upper gastrointestinal toxicity of rofecoxib and naproxen in patients with rheumatoid arthritis. VIGOR Study Group. N Engl J Med. 2000 Nov 23;343(21):1520-8, 2 p following 1528.
[33] |Mamdani M, Rochon PA, Juurlink DN, Kopp A, Anderson GM, Naglie G, Austin PC, Laupacis A. Observational study of upper gastrointestinal haemorrhage in elderly patients given selective cyclo-oxygenas-2 inhibitors or conventional non-steroidal anti-inflammatory drugs. BMJ. 2002 Sep 21; 325(7365):624.
[34] Rahme E, Marentette MA, Kong SX, Lelorier J. Use of NSAIDs, COX-2 inhibitors, and acetaminophen and associated coprescriptions of gastroprotective agents in an elderly population. Arthritis Rheum. 2002 Dec 15;47(6):595-602.
[35] Deeks JJ, Smith LA, Bradley MD. Efficacy, tolerability, and upper gastrointestinal safety of celecoxib for treatment of osteoarthritis and rheumatoid arthritis: systematic review of randomized controlled trials. BMJ. 2002 Sep 21;325(7365):619. Review.
[36] Pincus T, et al. A randomized, double-blind, crossover clinical trial of diclofenac plus misoprostol versus acetaminophen in patients with osteoarthritis of the hip or knee. Arthritis Rheum. 2001 Jul;44(7):1587-98.
[37] Felson D. The verdict favors nonsteroidal antiinflammatory drugs for treatment of osteoarthritis and a plea for more evidence on other treatments. Arthritis Rheum. 2001 Jul:44(7):1477-1480.
[38] Lohmander, LS, Dalen N, Englund G, et al. Intra-articular hyaluronan injections in the treatment of osteoarthritis of the knee: a randomized, double blind, placebo controlled multicentre trial. Hyaluronan Multicentre Trial Group. Ann Rheum Dis. 1996 Jul;55(7):424-31.
[39] Wobig M, Dickhut A, Maier R, Vetter G. Viscosupplementation with hylan G-F 20: a 26-week controlled trial of efficacy and safety in the osteoarthritic knee. Clin Ther. 1998 May-Jun;20(3):410-23.
[40] McAlindon TE, Gulin J, Felson DT. Glucosamine (GL) and chondroitin (CH) treatment for osteoarthritis of the knee or hip: Meta-analysis and quality assessment of clinical trials. Arthritis Rheum. 1998 Sept;41(9):S198, abstract #994.
[41] Reginster JY, et al. Long-term effects of glucosamine sulphate on osteoarthritis progression: a randomized, placebo-controlled clinical trial. Lancet. 2001 Jan 27;357(9252):251-6.
[42] Brittberg M, Lindahl A, Nilsson A, et al. Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation. N Engl J Med. 1993 Oct 6;331(14):889-95.
Posted: 3/20/2012


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State Farm Insurance Agent View Licenses
Across from the monument at 1st Baptist in downtown Opelika.Map & Directions Contact Us
Mon-Fri 8:30am to 5:00pm
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Banking, Mutual Funds, Annuities
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Banking, Mutual Funds, Annuities
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Opelika, AL 36801
Good condo insurance coverage works with in tandem with the condo association master policy. Get condo insurance basics here. Read more
Car manufacturers have rolled out many new car safety features in the last few years. Learn more about adaptive headlights, blind spot detection and more. Read more
Why won't your motorcycle start? This article will help you troubleshoot your problem so you can get back on the road where you belong. Read more
State Farm Bank, F.S.B., Bloomington, Illinois ("Bank"), is a Member FDIC and Equal Housing Lender. NMLS ID 139716. The other products offered by affiliate companies of State Farm Bank are not FDIC insured, not a State Farm Bank obligation or guaranteed by State Farm Bank, and may be subject to investment risk, including possible loss of principal invested. The Bank encourages any interested individual(s) to submit an application for any product(s) offered by the Bank. We also encourage you to obtain information regarding the Bank's underwriting standards for each type of credit or service offered by visiting statefarm.com or by contacting the Bank at 877-SF4-BANK (877-734-2265). Callers who are hearing or speech impaired should dial 711 or use a preferred Telecommunications Relay Service. To apply for a Bank product, you may also see your participating State Farm agent.
Life Insurance and annuities are issued by State Farm Life Insurance Company. (Not Licensed in MA, NY, and WI) State Farm Life and Accident Assurance Company (Licensed in New York and Wisconsin) Home Office, Bloomington, Illinois.
Investors should carefully consider investment objectives, risks, charges and expenses. This and other important information is contained in the fund prospectuses and summary prospectuses which can be obtained by visiting the prospectus page on statefarm.com. Read it carefully. AP2019/01/0054
State Farm VP Management Corp. is a separate entity from those State Farm entities which provide banking and insurance products. Investing involves risk, including potential for loss.
Neither State Farm nor its agents provide tax or legal advice. Please consult a tax or legal advisor for advice regarding your personal circumstances.

subset: commoncrawl


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It is hard to believe I am already beginning my 3rd year as a graduate student at Seattle Pacific University. I feel blessed to have the opportunity to be supported by both the School of Education and the Physics Department here on campus.
My Education coursework has given me insight into the world of education beyond the classroom and my work with the Physics department has helped me hone my skills as a researcher on the teaching and learning of a specific discipline. Because I have a broad background that spans scientific research as well as classroom teaching experience, this connection to both departments helps support my growth in the Physics Education Research community.
In the past, I earned undergraduate degrees in Physics and Astronomy from Mount Holyoke College, an M.S. in Physics from Clemson University, and obtained a Physics Teaching Credential at Chapman University. Professionally, I was a secondary educator for five years, three of which were spent teaching primarily physics courses to high school seniors. I received a fellowship from the Knowles Science Teaching Foundation, an incredible source of support and networking for novice teachers. It was during this time that I learned of a community that connected both research and education – the Physics Education Researchers at Seattle Pacific University.
My work now focuses on learning about energy in the context of the Physics Department's Energy Project. I began my work by observing the K-12 professional development courses offered by the Energy Project as an Interdisciplinary Research In STEM Education (I-RISE) scholar my first summer at SPU. I found myself drawn to spontaneous teacher discussions, in which teachers brought up social and political aspects of energy that did not correspond to canonical physics topics explicitly supported in the PD. This lead me to realize that while I was a high school teacher, I also taught two units on energy that failed to connect school learning of energy with energy discussed in society. I had inadvertently been missing the opportunity to connect sociopolitical energy concerns with physics energy concepts and in doing so, I left my students with two conflicting, separated views of energy. I want to help other teachers develop ways to connect these ideas for themselves, so that they can take those resources back to their classrooms. Dr. Rachel Scherr, Dr. Stamatis Vokos, and Dr. Andrew Lumpe have supported me in identifying a worthwhile research topic on learner ideas about energy and responsive energy instruction. My aim is to help reconnect those energy ideas for teachers (and students) so that learning about energy in physics sources will be more relevant outside of the classroom. My recent work has been presented at the 2013 American Association of Physics Teachers conference, as well as the 2013 Physics Education Research Conference. Relevant publications can be found here:
The author Abigail Daane is a current PhD student at SPU.


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Platform for Internet Content Selection
|computing dictionary
<world-wide web> (PICS) A standard for meta-data associated with World-Wide Web content, originally designed to help parents and teachers control what children access on the Internet, but also used for code signing and privacy. The PICS platform is one on which other rating services and filtering software have been built.
Acronym: PICS
(01 Jun 2001)
platelike atelectasis, plate of modiolus, platetrope, platform < Prev | Next > Platform Independent Graphical User Interface, plathelminth
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If this is not available for you out of the box in the settings page (details, content, plug-ins), you can enable it in about:flags, "click-to-play". You have to restart Chrome for it to take effect. As before, I really don't know why they removed it from the settings page in the first place.
In that same flags page you can also disallow the reading of third party cookies.
If you like this post, share it and subscribe to one of the RSS feeds so you don't miss the next one. In any case, check the related posts section below.
Enabling the Integrated Flash and Plugin Blocker in Google Chrome
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The iPhone SDK will not allow 3rd party apps to multitask or run background services. We've previously covered both initial developer Twitter-rage at this, and pundit counter-points. We've also covered Craig Hockenberry before -- the man who (perhaps poetically) develops Twitterrific for the Mac and jailbroken iPhones, and is now bringing it to the SDK.
Hockenberry, via his furbo.org blog, shares his experience on iPhone development and his views on the multitasking (non-?) issue.
To be blunt, I've never seen so many experts without a fricken' clue. If you haven't written code using the jailbreak tool chain, your opinions on the iPhone SDK, based entirely on what you see in a simulator, just aren't relevant. You might as well be explaining the nuances of brain surgery.
Wha-wha-wha-what? Please, allow Mr. Hockenberry to continue:
Twitterrific on the iPhone could definitely make use of a background process to gather new tweets. In fact, a prototype version of the software did just that. And it was a huge design failure: after doing XML queries every 5 minutes, the phone's battery was almost dead after 4 hours. In fact, the first thing I said after giving Gruber this test version was "don't use auto-refresh."
Hockenberry goes on to discuss the power demand problem of the radios, both EDGE and Wi-Fi, and the danger of even well-intentioned developers getting individually reasonable but collectively overwhelming access to background services. He does, however, expect that in a future release Apple may include some method of notifying network apps that the radios are being used (for example, by MobileMail Touch), and allowing brief TCP/IP connections during that period. Bottom-line, at the OS's discretion, not the individual apps'.
Sound reasonable? Sound crazy? Should Apple give unfettered access to everyone immediately an trust users to sort through it themselves? Or should Apple be as strict as possible from the get-go? What do you think?


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Oregon will honor marriages of same-sex couples who legally marry out of state
October 17, 2013
Today, state officials in Oregon announced that effective immediately, Oregon would equally honor the marriages of same-sex couples who legally marry out of state.
Oregon's Chief Operating Officer Michael Jordan issued a memo today to all state agencies explaining that legally married same-sex couples would be eligible for any state protections and responsibilities of marriage that different-sex couples receive. Jordan wrote:
Oregon agencies must recognize all out-of-state marriages for the purposes of administering state programs. That includes legal, same sex marriages performed in other states and countries.
The decision is a step forward for same-sex couples in Oregon - married same-sex couples will now be granted with the same respect as married different-sex couples, just as married non-gay couples are treated when they move between states.
But the decision also contributes to the already-confusing patchwork of federal and state laws and legal opinions that same-sex couples across the United States must navigate to protect their families and live their lives. No one should have to cross a state border to marry the person they love - and the news today does nothing to change the constitutional amendment that bans same-sex couples from marrying in Oregon. It underscores that it's time for marriage in Oregon.
The only surefire way for same-sex couples and their families to enjoy all of the protections and responsibilities of marriage - and be able to declare their love and commitment in the state where they live - is by overturning the constitutional amendment in the state and extending the freedom to marry to all couples.
Oregon United for Marriage is the coalition in the state working hard to overturn the anti-family amendment and replace it with an amendment that guarantees the freedom to marry to same-sex couples in Oregon. The organization has already collected thousands of signatures from fair-minded Oregonians who want same-sex couples to be able to share in the joys of marriage, and the state will be able to stand on the right side of history in November 2014 by voting for marriage.


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- In general, I passed on tasting Chardonnay and Merlot, because I have limited palate stamina and have little interest in those wines. However, as you will see below, I tasted a few of these wines when it seemed appropriate to do so.
It was NOT our goal to perform a forced march through Walla Walla wine tasting rooms. Rather, we tried to visit about 5 wineries a day, taking as much time as we wanted to talk with people, and to see some other sights (like the Fort Walla Walla Museum).
We visited a selection of wineries on the west side and south of town, and a couple at the airport; we did not hit the downtown tasting rooms or the east side wineries. I estimate we saw roughly a tenth of the total wineries in the greater Walla Walla area.
Keep in mind that the great January 2004 vine freeze destroyed roughly 80% of the Walla Walla grape vines, forcing many of the wineries to produce Columbia Valley wines, rather than Walla Walla wines, in 2004.
West Side
- Woodward Canyon: This winery is located on Rt 12, in Lowden, a 10-15 minute drive from downtown. They had numerous offerings of Merlot and Cabernet Sauvignon and blends for us to taste, and we found all of them to be very good to excellent wines. We started with their NV Columbia Valley Red ($17), which has dark fruit with leathery notes. This Cab-dominated blend has a rather unique ingredient grape, Barbera (11%), and it is a nice wine for the price. Their second label 2004 Nelms Road Cabernet Sauvignon ($21) is pretty good, but it did not compel me to buy. The 2003 Merlot ($39) is quite a lovely wine with dark chocolate on the nose; it has luscious dark fruit flavors and a very good finish. The 2002 Estate Red ($55) is dark and sultry, and came across as a beautiful wine. It is a blend of Cabernet Franc (39%), Merlot (38%) and Cabernet Sauvignon (23%). Their 2003 Artist Series #12 Cabernet Sauvignon ($44) brings together grapes from seven different vineyards to produce an outstanding wine that is both smooth and complex. We ended with the 2003 Columbia Valley Old Vines Cabernet Sauvignon ($75), a 100% varietal made from predominantly Champoux Vineyard grapes. This wine has a hint of spice on the nose and very rich flavors; it's a huge wine with great aging potential.
L'Ecole No 41: A few yards to the east you will see a nicely manicured lawn with a lovely old schoolhouse building. Unfortunately, I felt rather disappointed with some of the wines I tasted here. They had an extremely generous number of wines available for tasting, and I did not even attempt to try all of them. I tasted two (of the three) bottles of Semillon available that day. The 2005 Seven Hills Semillon ($19) has a crisp and pleasant floral aroma, and delivers a nice balance of fruit and acid. The 2004 Fries Vineyard Semillon ($19) has less of a floral aroma with perhaps a bit of diesel, and delivers more citrus on the finish. Jumping to the reds, I tried the 2004 Recess Red ($17), a blend of six different grapes, including a fair amount of Syrah (25%) and small amounts of Malbec and Carmenere. It comes across as a medium-light quaffer with bright fruit and light tannin; good, but it did not grab me as compelling. So I jumped right to the big blends, Perigee (which they served first) and Apogee. The 2003 Perigee ($44) is a 3-grape blend that shows some interesting complexity, but not enough body-fruit-finish to justify the price. This was the first time I tasted this wine and I was comparing it to Ensemble Cellars Release One ($48), which we tasted the previous evening (see below). The 2003 Apogee ($44) is a 4-grape blend that delivers bright fruit, but without that rich feeling I'd experienced with the 2001 vintage. It surprised me greatly that these wines did not compare well to other Walla Walla wines I tasted at this price point. (Word has it that L'Ecole No 41 has been steadily increasing production the past few years.) I finished up by tasting the 2004 Seven Hills Syrah ($36), which I found to be very nice, with good berry and spice on the nose and palate.
Reininger: Working our way back toward town, we stopped next at Reininger, where I was introduced to their second wine label, Helix. My first taste was the 2005 Helix Aspersa ($18), a blend of Viognier (60%) and Chardonnay (40%). The aromas of both grapes definitely come through; the wine is crisp with good acid, fruit and nice finish. However, my initial thought and final impressions were "Why would anyone want to ruin a decent Viognier by adding Chardonnay to it?" The 2005 Helix Rose' ($18), made entirely from Merlot, is nice and dry, and an altogether nice wine … for Rose' lovers, of course. The other Helix selection I tried was the 2003 Pomatia ($20), a 4-grape blend that is half Cabernet Sauvignon; it has some nice complexity in a medium-light wine. From here I moved to the standard Reininger label, starting with the 2003 RTW ($25), a 4-grape blend with over half being Syrah. It brings some pepper on the nose and bright fruit flavors with a good finish; however, I detected some intermediate bitterness on the palate. Their 2002 Walla Walla Valley Cabernet Sauvignon ($32) contains small amounts of Cabernet Franc and Carmenere, has a nice dark aroma, and delivers very good dark cherry fruit with some leather on the finish. The 2003 Walla Walla Valley Syrah ($32) has lots of fruit and pepper on the nose and the palate. Both of these last two wines were very nice.
Skylite: We stopped here, because the Reininger hostess said they made a very nice Viognier. Unfortunately, their new winery building/tasting room is not finished yet, and they were already sold out of their Viognier. (Apparently, they only made 50 cases of it.) The assistant winemaker suggested we try Amavi, because they have a really elegant Semillon.
Amavi: I was quite anxious to try their 2005 Columbia Valley Semillon ($20), and I was not disappointed. It has a beautifully crisp aroma, to which Eileen exclaimed, "It smells like sunshine." The wine has a nice creamy (but not flabby) texture that comes from 100% fermentation in neutral oak, and aging sur lie. Its flavors are rich with lovely lemony nuances, and it is all balanced with nice acidity. All in all, this is a very distinctive wine. Their 2004 Columbia Valley Syrah ($28) is very dark, with an awesome aroma; it is a big wine that delivers complex flavors without over extracted jaminess. This was the best Syrah for the price we tasted during this visit. The final wine we tasted here was the 2004 Columbia Valley Cabernet Sauvignon ($24), which has almost 23% Merlot and 2% Cabernet Franc. Its dark fruit, lovely texture and medium tannin made it one of the nicest Cabs we found for the price. They also have a high-end 2004 Les Collines Vineyard Syrah ($30), which is due to release in November; unfortunately, they were not offering tastes at this time. We really liked Amavi wines, and joined their wine club.
Whitman: It was getting late in the day and we were getting tired from a full day of sightseeing and tasting, so this was a quick stop. I tasted only one wine here, their 2005 Walla Walla Valley Viognier ($19), which has a lovely floral aroma, along with crisp citrusy fruit flavors.
South Side
- Skylite: On our way to the south side wineries, we stopped at their downtown tasting room at 10AM. Unfortunately, it wasn't open yet, and there was no sign indicating the hours of operation. So, we moved on to our first winery of the day.
Basel Cellars: We knew nothing about this winery, other than it opened at 10AM, so we headed 10 minutes south on Rt 125. Since we were the only tasters there, we were able to spend almost two hours with winemaker Trey Busch, who poured our tastes that morning, including some unreleased wines. The 2003 Claret ($24) is a Cab-Merlot-Syrah blend with good complex aromas, and medium+ body with cherry fruit, good acid and a nice finish. The 2004 Claret ($24, releasing in December) is a different blend altogether; it is lighter than the '03 and still a bit closed. I decided to try the 2004 Merlot ($24), which has 16% Cab Sauv blended in; it has nice red fruit aromas and tastes with some light tannin on the side. The 2003 Columbia Valley Cabernet Sauvignon ($32) has 16% Syrah. With dark fruit all the way, and a bit of mint or menthol hidden in there somewhere, it is a very good wine, starting with its complex aromas to its really long finish. As much as I liked the previous wines, I was even more thrilled by their 2003 Walla Walla Valley Red Wine ($36), a blend of Merlot (56%) and Cabernet Franc (44%). This wine is beautifully structured, with lovely dark fruit and medium tannin. The 2003 Merriment ($48) is a blend of Merlot (50%), Cabernet Sauvignon (45%) and Cabernet Franc (5%), and it delivers a very good, complex wine with firm tannin and bright fruit. We both loved these last two wines. The 2004 Columbia Valley Syrah ($42) was dark and rich with intense flavors without being jammy. However, we quickly discovered a deeper level of darkness to be found in Washington Syrah when we tried the (unreleased) 2004 Lewis Vineyard Reserve Syrah ($60) from the Yakima Valley, a HUGE wine in all dimensions. The wine is so dark, it appears black; the aroma is a mixture of dark fruit and grilled meat; the flavors are intense and the finish lasts forever. The wine is so big and well put together, we didn't notice that it packs a whopping 15.9% ABV. A limited amount of this killer Syrah was produced, and it is scheduled for release to their wine club members in September. (Oh, yes … we joined on the spot … and we did serious damage at this winery.) Before we left, Trey Busch made appointments for us at Isenhower and Rulo, which were not normally open that day. He also took us on a winery tour, and into a nearby vineyard to sample the ripeness of Cabernet Sauvignon grapes. This stop was the highlight of our visit.
Isenhower: We have friends in Gig Harbor, who love this winery, and they recommended we stop here; I'm glad we were able to do so. Our first wine here was the 2005 Snapdragon ($18), a blend of Rousanne (55%) and Viognier (45%). I've tasted this unique blend before, which smells floral and tropical (the Viognier), yet has some heaviness and spicy flavors (the Rousanne). We were lucky to be able to taste their 2004 Red Paintbrush ($26), which had previously been sold out (until an east coast distributor defaulted on their allocation). This smooth tasting blend of Merlot (80%), Cabernet Sauvignon (17%) and Syrah (3%) is made for easy drinking and delivers nice body with it. We next tried two samples of Syrah: 2004 Wild Alfalfa Syrah ($28) and 2004 River Beauty Syrah ($32). They are both dark and well made; however, the River Beauty grapes come from the Horse Heaven Hills, and it has noticeably more body and aging potential. The final wine we tasted was the 2004 Tapteil Vineyard Red Mountain Cabernet Sauvignon ($40), which has bright red fruit and medium tannin.
Pepper Bridge: We hadn't planned to stop here, but we had 45 minutes before our next appointment and we needed a place to have a quick bite of lunch. Note that although many wineries charge a modest $5 tasting fee, which applies against any wine purchase, Pepper Bridge had the highest tasting fee ($8) we encountered out there. They had only three wines to taste, and they were all big premium wines. The 2003 Walla Walla Valley Merlot ($45) has a wonderfully rich aroma, and intense flavors, but with some unidentified mid-to-back palate tastes at first. (This could have been an aftereffect of my hastily consumed lunch, however.) This Merlot is a big wine and needs food to do it justice. Their 2003 Walla Walla Valley Cabernet Sauvignon ($50), which contains small amounts of Merlot and Malbec, is big and lush with dark cherry aromas, intense flavors and a really long finish. The 2002 Walla Walla Valley Cabernet Sauvignon ($50) also contains small amounts of Merlot and Malbec, and is equally big and dark, but with somewhat less appeal than the '03. Although pleasant and seemingly knowledgeable, I was rather turned off by the hostess, who kept pushing issues of Wine Enthusiast (or was it Wine & Spirits?) magazine in front of me to show how much they liked these wines. The wines were terrific, but I would really prefer to have an intelligent discussion of the qualities of the wine, rather than being told that wine reviewer X gave them 92 points.
Rulo: This was a fun visit, because the owner-hostess was very engaging and had a great sense of humor; they also make really nice wines here. The first wine on the left was the 2004 Viognier ($18), which some folks feel is a strong candidate for Best Viognier in the Walla Walla area. It has everything I like in a good Viognier: engaging floral aroma, nice acidity, crisp fruit, and a lingering finish. I really liked this wine. Their next white wine, 2005 Combine ($15), is another unique blend of Sauvignon Blanc (82%) and Viognier (18%). It is neat and crisp, and it delivers the best of both varietals for me, floral aromas with lemony flavors. I broke my no-Chardonnay rule here, because our hostess wanted me to taste the difference between two of their vintages. The 2004 Sundance Vineyard Chardonnay ($20) is made from grapes grown in Matawa, north of the Tri-Cities area along the Columbia River. This wine has crisp fruit and minerals with more of an old world taste to it, and I preferred it to the next one. The 2005 Walla Walla Chardonnay ($20) is richer with more fat and butter, but is too much like most other domestic Chardonnay for my taste. The 2004 Syrah ($20) comes across as a very good wine for the price, but the 2003 Silo Syrah (aka Reserve, $25) is quite a stunner with more of just about everything, including a nice dose of black pepper. Unfortunately, they were out of this wine, and just happened to have an open bottle at hand. SIGH.
- Ensemble Cellars: This new winery, which released its first product in May 2006, is open by appointment only. It was actually our first stop of the trip, late in the day of our arrival. They produced a relatively small amount (250 cases) of a Bordeaux style blend that winemaker, Craig Nelsen, is trying to fashion after Ch. Margaux Bordeaux. The name Ensemble is significant in many respects. First, it reflects the winemaker's love for music and the fact that he is a classical violinist. Second, it reflects the careful blending of this wine, which spans two vintages and seven vineyards. The NV Release One Columbia Valley Red Wine ($48) is comprised of Cabernet Sauvignon (60%), Merlot (24%) and Cabernet Franc (16%), and is a blend of 2003 (68%) and 2004 (32%) vintages. This is a very polished and elegant wine with wonderful dark cherry flavors and lovely balance. Astute (or lucky) buyers were able to pre-purchase this wine at $38. We also tasted the unreleased NV Release Two Columbia Valley Red Wine ($tbd), which is a blend of three vintages (2003-2004-2005). Like its predecessor, it will be a beautiful wine upon release in May 2007. Moving forward, future releases of Ensemble Cellars wines will span three vintages, and will reach an annual production close to 350 cases. Note that these wines can only be purchased at the winery (either in person, by phone or FAX) or at Water to Wine, the wine shop in Gig Harbor that Craig Nelsen first opened in 1999.
Tamarack: In truth, we did not stop at this winery; it was on our list, but we ran out of time and did not get around to making an appointment for a mid-week visit. However, we just missed meeting the winemaker, who had been visiting Craig Nelsen at Ensemble Cellars. Fortunately, they left a small amount of 2003 DeBrul Vineyard Reserve ($40), which we tasted with Craig. This blend of Cabernet Sauvignon (62%), Merlot (31%) and Cabernet Franc (7%) starts with dark fruit aromas with some smoke and chocolate on the nose. It then delivers lush dark fruit flavors with some leather on the long finish.
Buty: We had heard very good things about this small winery. Unfortunately, it was closed … apparently they sold all of their wines this year.
Dunham Cellars: This was our final stop of the trip, and we actually arrived a few minutes after 4PM, their posted closing time. Since there were still two tasters inside, the hostess graciously welcomed us in. I started with the 2005 Walla Walla Rose' Wine ($26, but on sale for $19). This 100% Cabernet Franc dry Rose' wine is a light pink salmon with crisp fruit and floral notes. It was very nice, but somewhat hard to justify at the regular price. The 2004 Three Legged Red ($19) had a very nice aroma, but the wine seemed to be a bit sour and acidic. The 2004 Trutina ($24) was a richer tasting blend of Cabernet Sauvignon-Merlot-Cabernet Franc with a noticeably nicer and longer finish than the TLR. The 2002 Columbia Valley Cabernet Sauvignon VIII ($45) remains their flagship wine; it delivers dark fruit and mocha aromas, and dark cherry tastes. The 2003 Columbia Valley Syrah ($45) comes with an enticing dark and spicy aroma; it has very complex tastes of fruit and spice … very nice.
I hope you find these notes to be useful and interesting.
-- Clark


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Sunday, April 06, 2014
Are you voting or are you on vacation?
Posted by ecophilo at 7:06 AM
Labels: elections14
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A streetside glimpse of India from Bangalore - no paid news, no lobbying, no plants, no stringing along - just pure viewpoints. My own political education. Satire Alert (At times)! Because, nothing is permanent, only interim!
Posted by ecophilo at 7:06 AM
Labels: elections14
Government Software Systems Ltd
Resourcefulness and Indian business
Mopeds, mobiles, micro entrepreneurs
Brand India and the blogosphere
Real estate boom in India, Bangalore
Black to white...a long journey ahead
Reinventing oneself, Amitabh Bachchan
Will the world speak a single language
Weekend encounter, MLM specialist


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I'm going to take a small break from cycling to vent a bit...
The Republican campaign for president continues... but I have no interest. I gave up on the Republican party long ago.
Actually, I'm a Republican wanna-be. I want to vote for a party which is fiscally responsible, which balances its budget, which limits its federal involvement to things which the federal government is uniquely qualified to do like interstate commerce and international relations. I agree states should be granted broad freedom in their ability to decide on local matters, that competition between states is good, and that free market principles should be harnassed whenever externalities don't dominate. I have a strong appreciation of the tragedy of the commons. Further, I am a champion of individual freedom: I agree we should be able to express ourselves freely, travel freely, choose if and how we practice religion freely, and have input over the policies and actions of our government. These should be positions embraced by the Republican party.
But the Republican party really has little to do with these matters. Instead, it's just another face of the same old machine where money buys influence, influence used to drive the short-term profits of the few, virtually ignoring the long-term health of the nation. The fact the Republican Party wraps itself in the cloak of Christianity is the ultimate in hypocracy. This alone is sufficient reason to reject it.
This is nowhere more obvious than it is in the rhetoric on the public health debate. "Nobody should be required to pay for someone else's health care," I read over and over again. These people seem to have no issue with "public fire protection", or "public police protection", or "public military protection", or a "public road system", or in most cases even "public education system". But for some reason if I'm hit by a car and am bleeding to death on the street, my ability to pay is supposed to be assessed before I can be administered aid. Or if I'm stricken with a heart attack I'm supposed to be provide proof of insurance before my heartbeat is restored. It's all part of the inherent efficiencies of the free market.
Or perhaps this isn't their position. After all, it was Ronald Reagan who signed into law the Emergency Medical Treatment and Active Labor Act which requires emergency rooms on private and public hospitals to provide emergency care to people without regard for ability to pay. That care, of course, is passed on to those who are able to pay. This is socialized medicine in its purest form. In comparison, "ObamaCare" is it a laughable imitation.
So given this, that hospitals must care for those who can't pay for the service, there is immediately a direct public financial interest in helping people stay healthy, since emergency care is outrageously expensive (this is another matter, another problem; it's not obvious this needs be the case). This is in addition to the "well functioning society requires a healthy population" argument... an unhealthy population, like an uneducated one, is simply unable to provide for a competitive nation, any more than an unhealthy sports team is going to compete.
So what's the Bible say on the matter? The bible, many Republican supporters argue, is an important document for national policy. Well, it takes only a brief Google search to turn up the following verses from Luke 16:
19 "There was a rich man who was dressed in purple and fine linen and lived in luxury every day. 20 At his gate was laid a beggar named Lazarus, covered with sores 21 and longing to eat what fell from the rich man's table. Even the dogs came and licked his sores.
22 "The time came when the beggar died and the angels carried him to Abraham's side. The rich man also died and was buried. 23 In Hades, where he was in torment, he looked up and saw Abraham far away, with Lazarus by his side. 24 So he called to him, 'Father Abraham, have pity on me and send Lazarus to dip the tip of his finger in water and cool my tongue, because I am in agony in this fire.'
Seems pretty socialized to me: everyone has the responsibility to contribute to the needs of the sick, or else they will burn in Hades. It makes me question which Republican candidate Jesus would support....
Not that he'd support Obama, either, a president who has continued a needless state of war, perpetuated our destructive squandering of a precious resource (oil), and overseen a budget which is condemning future generations to supporting a crippling debt load so we can live an unsustainable lifestyle.
It's easy to despair.
added: As I write this, NPR is doing a story on the success of the Massachussetts health care law, which was supported for and signed by then-governor Romney. Rick Santorum has sharply criticized Romney for this. However, this doesn't stop Romney from prominently featuring "repeal Obamacare!" on his policy page.


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This online Flash interactive simulates the process of discovering new exoplanets using the transit method. Learners explore a simulated star field, record data, make measurements and do calculations to discover new planets. Instructional videos and... (View More) guides are included. (View Less)
This website features a range of interactive games, hands-on projects and fun facts about Earth, the Sun, our Solar System and Space.
This is a lesson that applys occultations to Saturn's Moon Enceladus. Learners will establish whether Saturn's small moon, Enceladus, has an atmosphere, whether that atmosphere is over the entire planet, and what creates Saturn's E-ring. The... (View More) activity is part of Project Spectra, a science and engineering program for middle-high school students, focusing on how light is used to explore the Solar System. (View Less)
This is an online sorting game that compares the lifetime risk of death from an asteroid impact to other threats. For example, are you more likely to be killed by an amusement park ride or an asteroid impact? It is part of the Killer Asteroids Web... (View More) Site. The site also features a background overview of the differences between asteroids and comets, information on different types of asteroids (rubble piles vs monoliths), a discussion of how at risk Earth really is to an asteroid or comet impact, and background information on light curves. (View Less)
Navigational tools and methods of early voyagers provide the background and contrast to the satellite images and models used today. Students complete mapping activities based on historical data from Columbus and Blith. Students will also use a... (View More) computer model of ocean currents to investigate the movement of objects drifting on the ocean surface. Note that this is lesson one of five on the Ocean Motion website. Each lesson investigates ocean surface circulation using satellite and model data and can be done independently. See Related URL's for links to the Ocean Motion Website which provide science background information, data resources, teacher material, student guides and a lesson matrix. (View Less)
Materials Cost: Free
This interactive, online activity traces the history of the telescope from Galileo's first look at the stars to the work of modern observatories. Learners will read about the milestones in telescope development, witness the interplay between... (View More) technological and scientific advances, glimpse the humanity of the inventors and astronomers behind the telescopes, find out what the telescopes discovered, as well as learn the science of light and optics. Students can work through the activity independently or in groups. Teachers may also choose to have students study a portion of the activity and then share their learning with the class. The science of light and telescopes is presented in the section called "Get to the root of it" that can be used for review, learning the basics, or remediation. Detailed teacher pages, identified as Teaching Tips on the title page of the activity, provide science background information, lesson plan ideas, related resources, and alignment with national education standards. (View Less)
Learners will use the inquiry process to explore the affect of atmosphere on the temperature of a planet. They create a model of the system to test. They then create a concept map of the planetary temperature system. The lesson models scientific... (View More) inquiry using the 5E instructional model and includes teacher notes, prerequisite concepts, common misconceptions, student journal and reading. This is lesson 10 in the Astro-Venture Astronomy Unit. The lessons are designed for educators to use in conjunction with the Astro-Venture multimedia modules. (View Less)
This interactive, online activity allows students to examine the Hubble Deep Field image and simulate the process astronomers have gone through to classify the objects in it. Students classify select objects in the image based on observable... (View More) properties such as color and shape. Students then compare their classifications to those made by astronomers. Upon completion of this activity, students will have classified objects in the Hubble Deep Field, described their characteristics, and used a table to display their data. Students can work through the activity independently or in groups. Teachers also may choose to have students prepare oral reports based on what they learned after performing the activity. Detailed teacher pages, identified as Teaching Tips on the title page of the activity, provide science background information, lesson plan ideas, related resources, and alignment with national education standards. This activity is part of the online exploration "The Hubble Deep Field Academy" that is available on the Amazing Space website. (View Less)
Learners will research and document some of the requirements for mounting an expedition to an asteroid; actively explore potential resources available to space travelers through research, assessment, team cooperation, and exploration simulations;... (View More) develop the background to make the connection between meteorite research and potential planetary resources; and map and core an edible asteroid. Materials lists, and advanced preparation and procedural tips are included. This is lesson 17 of 19 in Exploring Meteorite Mysteries. (View Less)
Materials Cost: $1 - $5 per group of students
This is a lesson about the effects of large impacts. Learners will use critical thinking skills to evaluate and apply data from a narrative to a scientific selection process, will demonstrate or visualize simulations of some of the effects of a huge... (View More) impact, and will write a point of view narrative. Materials and vocabulary lists, and advanced preparation and procedural tips are included. This is lesson 14 of 19 in Exploring Meteorite Mysteries. (View Less)
Materials Cost: Free


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DM2 Digital Video I/O Card
"DMediaPro DM2 and DMediaPro DM3 are Xtalk-based standard-definition and high-definition video I/O products for SGI Onyx2, SGI Tezro, SGI Onyx 3000 series, SGI Origin 2000, SGI Origin 3000 and SGI Octane2."
- TechPubs DM2/DM3 Owners Guide
- Supportfolio software download
DM3 Digital Video I/O Card
"The DMediaPro DM3 (XT-DIGVID) board transmits and receives uncompressed high-definition video and standard-definition video in real-time. The DMediaPro DM3 board can be installed and used with the SGI Onyx 350 dual-head graphics system and the SGI Tezro visual (deskside and rackmountable) workstations. In the future, the DMediaPro DM3 board (referred to as the DM3 board throughout this guide) will also be compatible with other SGI systems."
- DM3 Datasheet
- TechPubs DM3 Users Guide
- Supportfolio software download
DM5 Graphics-to-Video Output Card
DMediaPro DM5 for high-definition (HD) and standard-definition (SD) video graphics-to-video output is designed to be used in conjunction with appropriately-equipped workstations. A VPro V12 or equivalent Infinite Performance graphics pipe with Dual Channel Display (DCD) option is required. Appears in /usr/gfx/gfxinfo as "DM5 attached to Dual Channel 1".
- DM5 Datasheet
- TechPubs DM5 Graphics-to-Video-Out User's Guide
- Supportfolio DM5 software download
DM6 Digital Video I/O card
The DM6 (SD-DIGVID) is "a half-length PCI-bus ... board for real-time input and output of uncompressed SDTV signals. With the [DM6] a computer can handle 8 and 10 bit digital serial SDTV streams." The DM6 was available for both the SGI Octane and SGI Fuel, though they do not appear to be common in the aftermarket. The DM6 was an OEM product also offeres as the SDStation by DVS Digital Video Systems Gmbh, and can sometimes be found under that name on Internet auction sites.
Part numbers: 013-3745-001, 013-3745-002.
- DM6 Datasheet
- TechPubs DM6 Installation Guide
- Supportfolio DM6 software download
- Forum thread on DM6 found in a Fuel
Standard definition graphics to video output listed in SGI marketing martial (Tezro datasheet) but unreferenced in techpubs.sgi,con or elsewhere.
DM8 Audio Card
The DM8 is a digital audio card called the M-Audio Revolution 7.1 in OEM form.
DM10 "Audio and Video Subsystem"
DM10 is a PCI Firewire I/O card used in the SGI Fuel, SGI Tezro, SGI Onyx 350 and other systems with PCI slots.
- TechPubs DM10 Software Installation Note
DM12 Audio/Video Digital I/O Card
The DM12 appears to be a digital audio/video I/O board produced by OEM DVS Digital Video Systems Gmbh and offered for SGI's Prism workstation.
From the press release: "The DVS Centaurus® SD/HD/2K video board supports the 64-bit Linux® operating system. The Centaurus board will be available as the SGI® DMediaPro™ DM12 digital media option to the Silicon Graphics Prism visualization system. DM12 will provide the professional digital media interface for up to 2K (8-bit or 10-bit) input and output, with single and dual link HD-SDI capabilities including dual-link output for RGBA (4:4:4:4) or YUVA (4:2:2:4). The DM12 card will have eight channels of digital audio, which can either be embedded or configured with HD-SDI interfaces. The DM12 board will facilitate greatly increased processing speeds, offering application developers of digital video solutions significantly more performance for their products on the Silicon Graphics Prism system."
- SGI's DM12 press release
Specialized Cables
Several of the DMediaPro cards use special cables to connect to peripherals. An example would be the LVDS cables used to connect a DM2 or DM3 to a VBOB. This section will try to capture some of the details, as these cables are becoming harder to source as years go by.
The LVDS cables used to connect these cards to a VBOB use a 26-position male-to-male Centronics "Mini D Ribbon" or MDR. They are sometimes referred to as an MDR-26. In addition to the SGI parts, 3M part number 14526-EZ5B-050-02C (0.5 meters) can be used.
Forum member canavan supplied the following pinout for these cables in this forum post:
1 <> 14 2 <> 2 3 <> 23 4 <> 22 5 <> 21 6 <> 20 7 <> 19 8 <> 18 9 <> 17 10 <> 16 11 <> 15 12 <> 26 13 <> 25 24 <> 24
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