text:
This information is produced and provided by the National Cancer Institute (NCI). The information in this topic may have changed since it was written. For the most current information, contact the National Cancer Institute via the Internet web site at http://cancer.gov or call 1-800-4-CANCER.
Normal human body temperature displays a circadian rhythm. Body temperature is lowest in the predawn hours, at 36.1°C (97°F) or lower, and rises to 37.4°C (99.3°F) or higher in the afternoon. Normal body temperature is maintained by thermoregulatory mechanisms that balance heat loss with heat production.[1,2,3]
Abnormal elevations of temperature result from either hyperthermia or pyrexia (fever). Hyperthermia results from failure of thermal control mechanisms. In fever, thermoregulatory mechanisms are intact, but the hypothalamic set-point is elevated above normal by exogenous or endogenous pyrogens. There are three phases to fever. In the initiation phase, cutaneous vasoconstriction promotes heat retention and shivering generates additional heat. When the new (elevated) set-point is reached, heat production balances heat loss and shivering stops. With lowering of the set-point to normal, cutaneous vasodilatation promotes heat loss to the environment in the form of sweating. These same mechanisms maintain normal core body temperature in afebrile individuals.[1,2,3,4]
Response to fever varies with age. In older people, inadequate thermoregulatory mechanisms may contribute to hyperthermia and result in arrhythmias, ischemia, mental status changes, or heart failure from increased metabolic demands. In children between the ages of 6 months and 6 years, febrile convulsions may occur.
In this summary, unless otherwise stated, evidence and practice issues as they relate to adults are discussed. The evidence and application to practice related to children may differ significantly from information related to adults. When specific information about the care of children is available, it is summarized under its own heading.
The major causes of fever in cancer patients include infection, tumor (also known as paraneoplastic fever), drugs (allergic or hypersensitivity reactions), blood product transfusion, and graft-versus-host disease (GVHD).[2,3,4,5,6,7,8] Infection is a particularly important cause in the neutropenic host, given its high frequency (almost two-thirds of patients) and potentially fatal outcome. Whereas gram-negative infections predominated as the cause of neutropenic fever in cancer patients in the 1970s and early 1980s, gram-positive infections, mainly streptococci and coagulase staphylococci, have predominated since. The increased incidence of staphylococcal and streptococcal infections relates to the use of intravascular devices, severe mucositis due to high-dose chemotherapy, and prophylactic antibiotic therapy with fluoroquinolones. Although fluoroquinolone use has not decreased the morbidity or mortality of neutropenic fever, it has resulted in increased incidence of resistant gram-negative bacteremia.[9] Many consider paraneoplastic fever to be more common in primary tumors such as renal cell carcinomas and lymphomas, but available data suggest that it occurs in tumors of diverse primary sites.[2] Hypersensitivity reactions, pyrogen production, primary cytokine production and tumor necrosis with secondary cytokine production are among the postulated causes of tumor fever. Drug causes of fever include a variety of cytotoxic chemotherapy agents, biologic response modifiers, vancomycin, amphotericin, and multiple other medications. Tumor-associated fevers may be cyclic, occur at a specific time of the day, or be intermittent, alternating with afebrile periods lasting days or weeks.[3,4] Fever pattern does not differentiate drug-associated fever from other causes of fever, except when the temporal relationship is unambiguous. For many drugs, a highly variable lag time between the initiation of the offending agent and the onset of fever masks the causative relationship.[4,6,7,10]
Other etiologies of fever in the cancer patient include drug withdrawal (i.e., opioids, benzodiazepines), neuroleptic malignant syndrome (NMS), obstruction of a viscus (i.e., bladder, bowel, kidney), and tumor embolization. Comorbid medical conditions such as thrombosis, connective tissue disorders, and central nervous system bleeds or strokes may also produce fever.[4] The differential diagnosis of fever in the cancer patient is extensive, and differentiating infection from other causes may be difficult. From a palliative perspective, establishing a fever-specific diagnosis is important, as the specific diagnosis impacts management, comfort, and patient prognosis.
Assessment of fever requires careful history taking, medication review, and a physical examination that includes all major body systems. Individuals with suspected infection, especially those with neutropenic fever, should undergo meticulous evaluation of the skin, all body orifices (i.e., mouth, ears, nose, throat, urethra, vagina, rectum), finger stick and venipuncture sites, biopsy sites, and skin folds (i.e., breasts, axilla, groin). Oral assessment includes evaluation of the teeth, gingiva, tongue, floor of the mouth, nasopharynx, and sinuses. The perirectal area is a common source of infection, especially in individuals with leukemia. Vascular access devices (VAD) and other artificial indwelling devices (i.e., percutaneous nephrostomy tubes, biliary drainage tubes, gastrostomy or jejunostomy tubes) are other commonly implicated sources of infection. Urine, sputum, and blood cultures (peripheral and from ports or lumens of VADs) and radiographic imaging with chest radiography as directed by these findings complete the initial evaluation. Individuals undergoing cytotoxic chemotherapy should be instructed to seek immediate medical attention if they develop fever when neutrophil counts are low or declining. Frequent reassessment, including physical examination, is especially important in the neutropenic host, as signs and symptoms of infection may be minimal. Evaluation for recurrent or progressive tumor can be performed at the same time as evaluation for potential infection and other causes of fever.[3]
The presence of fever is associated with the potential metabolic consequences of dehydration and increased metabolic demand. Effects may be especially pronounced in debilitated cancer patients and include uncomfortable constitutional symptoms such as fatigue, myalgias, diaphoresis, and chills. Potential interventions for fever management include primary interventions directed at the underlying cause, hydration with parenteral fluids or by hypodermoclysis, nutritional support, and nonspecific palliative measures. The specific interventions utilized are determined by the patient's location in the disease trajectory and patient-determined goals of care. Some patients near the end of life may decide not to treat the underlying cause. For example, patients with advanced cancer may decline treatment of pneumonia or other infections but still seek nonspecific palliative measures and hydration to optimize quality of life. Alternatively, others may elect antibiotic therapy for the palliation of symptoms such as cough, fever, dyspnea, or abscess pain. (Refer to the Nonspecific Interventions for Palliation of Fever section of this summary for more information.)
Primary Interventions
Infection-associated fever
Effective antibiotic treatment results in palliation of fever-associated constitutional symptoms, as well as palliation of site-specific symptoms such as cough secondary to pneumonia or localized pain due to abscess formation. For febrile neutropenic patients (granulocyte count <500), immediate initiation of broad-spectrum antibiotic treatment is imperative, as the mortality rate is 70% for patients not receiving antibiotics within 48 hours. For the purposes of neutropenia, fever is defined as a single temperature elevation above 38.5°C or three elevations above 38°C in a 24-hour period.[4]
Since the cause of neutropenic fever is not documented in 50% to 70% of patients, antibiotic use is guided by knowledge of the treating institution's antimicrobial spectrum and antibiotic resistance pattern, as well as the suspected cause. There is no consensus on the particular antibiotic or combination of antibiotics to be used, but empiric antibiotic therapy generally falls into one of four protocols:
When multiple-lumen catheters are present, antibiotic therapy should be rotated through each lumen. Bacteriostatic antibiotics (i.e., tetracycline, erythromycin, chloramphenicol) are not beneficial in the absence of granulocytes, which, when given concomitantly, reduce the efficacy of the bactericidal antibiotics.[4,11]
Treatment regimens are further modified by the duration of fever and individual patient risk factors such as the presence of central lines or other artificial devices, history of steroid use, and history of injection drug use. Various investigators have developed models predicting risk groups of febrile neutropenia, with implications for management strategies. Therapeutic options under evaluation include early hospital discharge, home intravenous antibiotic therapy, and oral antibiotic regimens. A subset of these studies focus on the pediatric population. Because of rapid changes in the field, the reader is directed to specialized sources for specific management recommendations of febrile neutropenia.[12,13,14]
After a specific pathogen is isolated, antibiotic therapy is modified to provide optimal therapeutic response with minimal toxicity. Broad-spectrum coverage must be maintained to prevent secondary bacterial and fungal infections. Antibiotic therapy is usually discontinued after 5 to 7 days provided that the patient's granulocyte count exceeds 500 and the patient remains free of fever and infection. There is no consensus as to appropriate management in cases of persistent granulocytopenia when the patient is afebrile. Some advocate continued therapy, whereas others favor discontinuing antibiotics once the patient stabilizes. Empirical antifungal therapy is often added if a neutropenic patient remains febrile after 1 week of broad-spectrum antibiotics or has recurrent fever, since continued granulocytopenia is usually associated with the development of nonbacterial opportunistic infections, particularly those caused by Candida and Aspergillus. Prolonged therapy (>10–14 days) is indicated in the patient with a residual focus of bacterial or mycotic infection. Amphotericin B is usually the agent of choice. Alternative antifungal agents (5-fluorocytosine, miconazole, fluconazole, or itraconazole) are indicated when organisms develop resistance to amphotericin B.
Acyclovir is the drug of choice in the treatment of herpes simplex or varicella zoster viral infection. Ganciclovir has activity against cytomegalovirus. Both agents can be used prophylactically in the management of patients at high risk for these infections. Foscarnet is useful in the treatment of cytomegalovirus and acyclovir-resistant herpes simplex virus.
Paraneoplastic fever
When available, the best management of tumor-associated fevers is treatment of the underlying neoplasm with definitive antineoplastic therapies. In the absence of effective antineoplastic therapy, nonsteroidal anti-inflammatory drugs (NSAIDs) are a mainstay of treatment. Naproxen may preferentially control paraneoplastic fever relative to other NSAIDs or acetaminophen. Response to naproxen has been considered diagnostic of tumor fever; however, efficacy of naproxen and other NSAIDs for infection-related fever is a common clinical observation. Release of tumor fever may respond to treatment with a structurally different NSAID.
Drug-associated fever
The occurrence of fever is predictable for some drugs, such as biologic response modifiers, amphotericin B, and bleomycin. For many other drugs, drug fever is a diagnosis of exclusion. Drug-associated fever responds to cessation of the offending agent, when possible. Fever and related symptoms with biologic response modifier administration is type-, route-, dose-, and schedule-dependent. These factors may sometimes be altered for fever control without sacrificing efficacy. Fever may also be attenuated by the use of acetaminophen, nonsteroidal anti-inflammatory, and steroid premedication. The same may be true for fever associated with some cytotoxic agents and antimicrobials (i.e., amphotericin).[6,7,10] It is common clinical practice to administer meperidine to attenuate severe chills associated with a febrile reaction, although empirical data confirming its efficacy are not available.
Neuroleptic malignant syndrome
Neuroleptic malignant syndrome (NMS) is a rare but potentially fatal syndrome that may develop during treatment with neuroleptic drugs for conditions such as psychotic disorders, delirium, nausea, and vomiting. It is marked by fever, rigidity, confusion, and autonomic instability, as well as by elevations in white blood cell count, creatinine phosphokinase, and urine myoglobin. NMS should be considered in the differential diagnosis of the delirious patient receiving neuroleptic agents who develops rigidity and whose condition does not improve on neuroleptics (e.g., haloperidol). Treatment of NMS includes discontinuation of neuroleptic agents, supportive measures, and occasionally, administration of bromocriptine or dantrolene. (Refer to the PDQ summary on Delirium for more information.)
Blood product–associated fever
Suspected febrile reactions can be minimized by the use of leukocyte-depleted or irradiated blood products, when clinically appropriate. Common clinical practice includes premedication with acetaminophen and diphenhydramine.[8]
Nonspecific Interventions for Palliation of Fever
Along with treatment of the underlying cause, comfort measures are helpful in alleviating the distress that accompanies fever, chills, and sweats. During febrile episodes, increasing a patient's fluid intake, removing excess clothing and linens, and tepid water bathing/sponging may provide relief. Results of a pediatric randomized placebo-controlled trial of sponging with ice water, isopropyl alcohol, or tepid water, with or without acetaminophen, demonstrated that all combinations enhanced fever control. Comfort was greatest in children receiving a placebo or sponging, followed by those who received acetaminophen combined with tepid-water sponging. Sponging with either ice water or isopropyl alcohol, with or without acetaminophen, resulted in the greatest discomfort.[15] During periods of chills, replacing wet blankets with warm, dry blankets, keeping patients out of drafts, and adjusting ambient room temperature may also improve patient comfort.
Symptomatic relief of persistent or intermittent fevers can be aided by the use of NSAIDs (e.g., naproxen) or acetaminophen.[15] Aspirin may also be effective in reducing fever but should be used with caution in patients with Hodgkin lymphoma and cancer patients at risk for thrombocytopenia. Because of the associated risk of Reye syndrome, aspirin is not recommended in patients with fever.[4]
Sweats and hot flashes are common in cancer survivors, from those in the adjuvant setting to those living with advanced disease. Pathophysiologic mechanisms are complex. Treatment options are broad-based, including hormonal agents, nonhormonal pharmacotherapies, and diverse integrative medicine modalities.[1]
Physiologically, sweating mediates core body temperature by producing transdermal evaporative heat loss.[2,3] Sweating occurs in disease states such as fever and in nondisease states such as warm environments, exercise, and menopause. Limited data suggest that sweating occurs in 14% to 16% of advanced cancer patients receiving palliative care, with severity typically rated as moderate to severe.[4,5,6]
Sweating is part of the hot flash complex that characterizes the vasomotor instability of menopause. Hot flashes occur in approximately two-thirds of postmenopausal women with a breast cancer history and are associated with night sweats in 44%.[7,8] For most breast cancer and prostate cancer patients, hot flash intensity is moderate to severe. Distressing hot flashes appear to be less frequent in postmenopausal women with nonbreast cancer.
Approximately 20% of women without breast cancer seek medical treatment for postmenopausal symptoms, including symptoms related to vasomotor instability.[9] Vasomotor symptoms resolve spontaneously in most patients in this population, with only 20% of affected women reporting significant hot flashes 4 years after the last menses.[9] There are no comparable data for women with metastatic breast cancer. Three-quarters of men with locally advanced or metastatic prostate cancer treated with medical or surgical orchiectomy experience hot flashes.[10]
Sweats in the cancer patient may be associated with the tumor, its treatment, or unrelated (comorbid) conditions. Sweats are characteristic of certain primary tumor types such as Hodgkin lymphoma, pheochromocytoma, and functional neuroendocrine tumors (i.e., secretory carcinoids). Other causes include fever, menopause, castration (male), drugs, hypothalamic disturbances, and primary disorders of sweating. Causes of menopause include natural menopause, surgical menopause, or chemical menopause, which in the cancer patient may be caused by cytotoxic chemotherapy, radiation, or androgen treatment. Causes of "male menopause" include orchiectomy, gonadotropin-releasing hormone use, or estrogen use. Drug-associated causes of sweats include tamoxifen, aromatase inhibitors, opioids, tricyclic antidepressants, and steroids. Women who are extensive metabolizers of tamoxifen related to CYP2D6 may have more severe hot flashes than those who are poor metabolizers.[11] Distinct from menopausal effects, hormonal therapies, biologic response modifiers, and cytotoxic agents associated with fever secondarily cause sweats.
As with interventions for fever, primary interventions directed at the underlying cause of sweats or hot flashes form the basis of management. In the absence of effective therapy or when onset is delayed, nonspecific palliative interventions are key.
The primary interventions for fever-associated sweats are those directed at the underlying cause of the fever (refer to the Primary Interventions for fever section for more information). Effective antineoplastic therapies control the sweats associated with tumor recurrence or progression. Somatostatin analogs are a primary treatment for flushes and sweats associated with some neuroendocrine tumors.
Hot flashes
Hormone replacement therapy
Estrogen replacement effectively controls hot flashes associated with biologic or treatment-associated postmenopausal states in women. The proposed mechanism of action of estrogen replacement on hot flash amelioration is by raising the core body temperature sweating threshold;[12][Level of evidence: I] however, many women have relative or absolute contraindications to estrogen replacement. Physicians and breast cancer survivors often think there is an increased risk of breast cancer recurrence or de novo breast malignancy with hormone replacement therapies and defer hormonal management of postmenopausal symptoms. Methodologically strong data evaluating the risk of breast cancer associated with hormone replacement therapy in healthy women have been minimal, despite strong basic science considerations suggesting the possibility of such a risk.[13]
In May 2002, the Women's Health Initiative (WHI), a large, randomized, placebo-controlled trial of the risks and benefits of estrogen plus progestin in healthy postmenopausal women, was stopped prematurely at a mean follow-up of 5.2 years (±1.3) because of the detection of a 1.26-fold increased breast cancer risk (95% confidence interval [CI], 1.00–1.59) in women receiving hormone replacement therapy. Tumors among women in the hormone replacement therapy group were slightly larger and more advanced than in the placebo group, with a substantial and statistically significant rise in the percentage of abnormal mammograms at first annual screening; such a rise might hinder breast cancer diagnosis and account for the later stage at diagnosis.[14,15][Level of evidence: I] These results are supported by a population-based case-control study suggesting a 1.7-fold (95% CI, 1.3–2.2) increased risk of breast cancer in women using combined hormone replacement therapy. The risk of invasive lobular carcinoma was increased 2.7-fold (95% CI, 1.7–4.3), the risk of invasive ductal carcinoma was increased 1.5-fold (95% CI, 1.1–2.0), and the risk of estrogen receptor–positive/progesterone receptor–positive breast cancer was increased 2.0-fold (95% CI, 1.5–2.7). Increased risk was highest for invasive lobular tumors and in women who used hormone replacement therapy for longer periods of time. Risk was not increased with unopposed estrogen therapy.[16]
The very limited data available do not indicate an increased risk of breast cancer recurrence with single-agent estrogen use in patients with a history of breast cancer.[17,18] A series of double-blind placebo-controlled trials suggests that low-dose megestrol acetate (i.e., 20 mg by mouth twice a day) and selective serotonin reuptake inhibitors (SSRIs) are among the more promising agents for hot flash management in this population. Limited data suggest that brief cycles of intramuscular depot medroxyprogesterone acetate also play a role in the management of hot flashes.[19][Level of evidence: I] Risk associated with progestin use is unknown.[13]
Other pharmacologic interventions
Numerous nonestrogenic, pharmacologic treatment interventions for hot flash management in women with a history of breast cancer and in some men who have undergone androgen deprivation therapy have been evaluated. Options with reported efficacy include androgens, progestational agents, gabapentin, SSRIs, selective serotonin norepinephrine inhibitors, alpha adrenergic agonists (e.g., methyldopa, clonidine), beta-blockers, and veralipride (an antidopaminergic agent). Inferior efficacy, lack of large definitive studies, and potential side effects limit the use of many of these agents.[20,21,22][Level of evidence: I]
Agents that have been found to be helpful in large, randomized, placebo-controlled clinical trials include venlafaxine, paroxetine, citalopram, fluoxetine, gabapentin, pregabalin, and clonidine.[20,21,22] These agents demonstrate a 40% to 60% reduction in hot flash frequency and score (a measure combining severity and frequency).[23] Agents conferring a 55% to 60% reduction in hot flashes are venlafaxine extended release, 75 mg daily;[24] paroxetine, 12.5 mg controlled release [25] or 10 mg daily;[26] gabapentin, 300 mg tid;[27,28][Level of evidence: I][29][Level of evidence: II] and pregabalin, 75 mg bid.[30][Level of evidence: I] Other effective agents resulting in about a 50% reduction in hot flashes include citalopram, 10 to 20 mg per day, which was studied in clinical trial NCCTG-N05C9;[31][Level of evidence: I] and fluoxetine, 20 mg per day.[21] Clonidine, 0.1 mg transdermal [32] or oral daily,[33][Level of evidence: I] can reduce hot flashes by about 40%.
One study compared the efficacy and patient preference of venlafaxine, 75 mg, once daily to gabapentin, 300 mg, 3 times per day for the reduction of hot flashes. Sixty-six women with histories of breast cancer were randomly assigned in an open-label fashion to receive venlafaxine or gabapentin for 4 weeks; after a 2-week washout period, they received the opposite treatment for an additional 4 weeks. Both treatments reduced hot flash scores (severity multiplied by frequency) by about 66%. However, significantly more women preferred venlafaxine over gabapentin (68% vs. 32%, respectively).[34]
A study using citalopram to evaluate hot flashes examined how much of a reduction in hot flashes was needed to have a positive impact on activities of daily living and general health-related quality of life.[35] The authors reported that hot flashes had to be reduced at least 46% for women to report significant improvements in the degree of bother they experienced in daily activities.
Agents that have been evaluated in phase II trials but have not shown efficacy include bupropion,[36] aprepitant,[37] and desipramine.[38][Level of evidence: II] Interestingly, these agents do not primarily modulate serotonin. In addition, randomized clinical trials with sertraline have not provided convincing evidence of its efficacy in hot flash management.[39,40,41][Level of evidence: I]
If nighttime hot flashes or night sweats are a particular problem without causing much bother during daytime, strategies to simultaneously improve sleep and hot flashes are in order. Limited data exist related to effective treatments that can target both symptoms. One pilot trial evaluated mirtazapine (a tetracyclic antidepressant that mainly impacts serotonin) for hot flashes because it is often prescribed for sleep difficulties. Twenty-two women were titrated up to 30 mg per day of mirtazapine at bedtime over a 3-week period; then they could choose 15 mg or 30 mg at bedtime daily for the fourth week. Hot flashes were reduced about 53% in this nonrandomized trial, and women were statistically significantly satisfied with their hot flash control.[42] However, only 16 of the 22 women stayed on the agent for the entire study period because of excessive grogginess. Therefore, although this agent could be further studied in a larger randomized trial, it would be particularly important to evaluate the risk/benefit ratio.
Trazodone is another possible agent to use for nighttime hot flashes, based on clinical experience. Trazodone, an atypical antidepressant that is often used as a sleeping aid, has anecdotally been shown to be particularly helpful in patients with nocturnal hot flashes. Doses range from 50 mg to 300 mg. Clinical experience suggests that trazodone can help patients fall asleep and can control hot flashes during the night, helping them to stay asleep. Trazodone is a tricyclic antidepressant and, as such, would not be expected to have a great impact on hot flashes: one open-label pilot trial conducted with a tricyclic antidepressant, desipramine, as a proof-of-principle study did not show a benefit.[38] However, this study has not been replicated. The effect of trazodone on sleep may be so profound that hot flashes are not bothersome; this hypothesis needs further study.
Side effects for antidepressant agents in the doses used to treat hot flashes are minimal in the short term and primarily include nausea, sedation, dry mouth, and appetite suppression or stimulation. In the long term, the prevalence of decreases in sexual function with SSRIs at doses used to treat hot flashes is not known. The anticonvulsants gabapentin and pregabalin can cause sedation, dizziness, and difficulty concentrating, while clonidine can cause dry mouth, sedation, constipation, and insomnia.[27,28,30][Level of evidence: I] Patients respond as individuals to both the efficacy and the toxicity of various medications. Therefore, careful assessment and tailored treatment chosen collaboratively by provider and health care consumer are needed.
Data indicate that if one medication is not helpful for an individual, switching to another medication—whether a different antidepressant or gabapentin—may be worthwhile. In a randomized phase III trial (NCCTG-N03C5) of gabapentin alone versus gabapentin in conjunction with an antidepressant in women who had inadequate control of their hot flashes with an antidepressant alone,[43][Level of evidence: I] gabapentin use resulted in an approximately 50% median reduction in hot flash frequency and score, regardless of whether the antidepressant was continued. In other words, for women who were using antidepressants exclusively for the management of hot flashes that were inadequately controlled, initiation of gabapentin with discontinuation of the antidepressant produced results equal to those obtained with combined therapy, resulting in the need for fewer medications. Similarly, in a pilot study of women receiving inadequate benefit from venlafaxine for hot flash reduction, switching to open-label citalopram, 20 mg per day, resulted in a 50% reduction in hot flash frequency and score.[44]
Drug interactions
Many of the SSRIs can inhibit the cytochrome P450 enzymes involved in the metabolism of tamoxifen, which is commonly used in the treatment of breast cancer. When SSRIs are being used, drug-drug interactions should be noted. Tamoxifen, used in the management of breast cancer, is metabolized by the cytochrome P450 enzyme system, specifically CYP2D6. Wild-type CYP2D6 metabolizes tamoxifen to an active metabolite, 4-hydroxy-N-desmethyl-tamoxifen, also known as endoxifen. A prospective trial evaluating the effects of the coadministration of tamoxifen and paroxetine, a CYP2D6 inhibitor, on tamoxifen metabolism, found that paroxetine coadministration resulted in decreased concentrations of endoxifen. The magnitude of decrease was greater in women with the wild-type CYP2D6 genotype than in those with a variant genotype (P = .03).[45][Level of evidence: II]
In a prospective observational study of 80 women initiating adjuvant tamoxifen therapy for newly diagnosed breast cancer, variant CYP2D6 genotypes and concomitant use of SSRI CYP2D6 inhibitors resulted in reduced endoxifen levels. Variant CYP2D6 genotypes do not produce functional CYP2D6 enzymes.[46][Level of evidence: II] Since this study was published, several researchers have been evaluating the clinical implications of this finding.[47];[48,49,50][Level of evidence: II] One study followed more than 1,300 women for a median of 6.3 years and concluded that women who were poor metabolizers or heterozygous extensive/intermediate metabolizers (hence, less CYP2D6 activity) had higher rates of recurrence, worse event-free survival, and worse disease-free survival than did women who were extensive metabolizers.[49] Similarly, a retrospective cohort study of more than 2,400 women in Ontario who were being treated with tamoxifen and had overlapping treatment with an SSRI has been completed. Authors concluded that women who concomitantly used paroxetine and tamoxifen had an increased risk of death that was proportionate to the amount of time they used these agents together.[50][Level of evidence: II] Clinical implications of these changes and of other CYP2D6 genotypes [51] have not yet been elucidated, but the pharmacokinetic interaction between tamoxifen and the newer antidepressants used to treat hot flashes merits further study.[52] Likewise, the risk of soy phytoestrogen use on breast cancer recurrence and/or progression has not yet been clarified. Soy phytoestrogens are weak estrogens found in plant foods. In vitro models suggest that these compounds have a biphasic effect on mammary cell proliferation that is dependent on intracellular concentrations of phytoestrogen and estradiol.[53]
Behavioral methods
Behavioral interventions as a primary or adjunctive modality may also play a role in hot flash management. Core body temperature has been shown to increase before a hot flash;[54] therefore, interventions to keep body temperature down could improve hot flash management. Some methods of controlling body temperature include the use of loose-fitting cotton clothing as well as the use of fans and open windows to keep air moving. Based on the theory that serotonin may be involved as a central hot flash trigger, behavioral interventions such as stress management may modulate serotonin, causing a decrease in hot flashes. Relaxation training and slow, deep breathing [55,56] have been found to decrease hot flash intensity by as much as 40% to 50% in controlled pilot trials. More research with well-designed control arms is needed to further clarify the main effect of such behavioral treatments as well as the additive and synergistic effects with other treatments. One pilot study also found that self-hypnosis, utilizing cooling suggestions, reduced hot flash scores an average of 68%.[57][Level of evidence: I] Self-hypnosis is being studied further in larger controlled trials as well as in combination with low-dose antidepressants.
Future research on hot flash management may be aided by the development of psychometrically sound assessment tools such as the Hot Flash Related Daily Interference Scale, which evaluates the impact of hot flashes on a wide variety of daily activities.[58]
Integrative approaches
Herbs/dietary supplements
Numerous herbs and dietary supplements are popularly used for hot flash reduction. Several of these substances have not been well studied in rigorous clinical trials. Furthermore, the biologic activity of various over-the-counter supplements has yet to be determined and is far from standardized. Some of the more well-studied agents include soy phytoestrogen, black cohosh, and vitamin E.
Vitamin E, 400 IU twice a day, appears to confer a modest reduction in hot flashes that is only slightly better than that seen with placebo. The reduction in hot flashes is roughly 35% to 40%.[59,60][Level of evidence: I]
Soy has been a dietary supplement of interest for decreasing menopausal symptoms and breast cancer for some time. The interest comes primarily from association studies of a high-soy diet and decreased breast cancer/menopausal symptoms in Asia. Soy is an isoflavone, which is part of a much larger class of plant compounds called flavonoids. Three types of isoflavones are found in soy products:
Isoflavones are often referred to as phytoestrogens or plant-based estrogens because they have been shown, in cell line and animal studies, to have the ability to bind with the estrogen receptor.[61]
There is confusion about the safety of these plant-based estrogens because these agents can have properties that can cause estrogen-like effects in some cells, causing them to proliferate (divide and grow); while in other cells, isoflavones can stop or block estrogen effects, causing unwanted cells to not grow or even die. There is continuing debate about the following questions:[62]
Definitive answers to these questions are not known, but phytoestrogens continue to be investigated for chemopreventive properties. On the other hand, soy has been well studied in numerous randomized, placebo-controlled trials for its effects on reducing hot flashes.[63,64,65,66,67][Level of evidence: I] Most of those trials show that soy is no better than a placebo in reducing hot flashes.[68][Level of evidence: I][69] Currently, there are no compelling data that would inspire the use of soy for hot flash management.
Similarly, trials of black cohosh that have been well designed with a randomized, placebo-controlled arm have also found that black cohosh is no better than a placebo in reducing hot flashes.[67,70,71][Level of evidence: I] Black cohosh used to be thought of as having estrogenic properties, but it is now known that it acts on serotonin receptors, as discussed at the Workshop on the Safety of Black Cohosh in Clinical Studies. One study evaluated black cohosh, red clover, estrogen and progesterone, and placebo in a randomized, double-blind trial.[72][Level of evidence: I] Each treatment arm was small (n = 22); however, over 12 months, hot flashes were reduced 34% by black cohosh, 57% by red clover, 63% by placebo, and 94% by hormone therapy. Of note, adherence rates were reported to be about 89% over the four groups during this long-term study. At 12 months, physiologic markers such as endometrial thickness, estradiol, estrone, follicle-stimulating hormone, sex hormone–binding globulin, and liver function tests were not statistically different for those on either red clover or black cohosh, compared with those on placebo. However, because these groups were small, the power for this secondary analysis was not reported, and it was likely underpowered to detect important differences.
Flaxseed is a plant that is part of the genus Linum, native to the area around the eastern Mediterranean and India. Flaxseed is a rich source of lignans and omega 3 fatty acids. Lignans found in flaxseed are called secoisolariciresinol diglucoside (SDG) and alpha-linolenic acid (ALA). Flaxseed is also a source of fiber. Lignans are a type of phytoestrogen (plant estrogen) that, like soy, is thought to have estrogen agonist-antagonist effects as well as antioxidant properties. Lignans are converted by colonic bacteria to enterodiol and enterolactone, which are metabolites believed to have important physiological properties such as decreasing cell proliferation and inhibiting aromatase, 5-alpha reductase, and 17-beta hydroxysteroid activity. Cell line studies have shown properties of aromatase inhibition with enterolactone but less so with enterodiol.[73] It is thought that these properties can reduce the risk of hormone-sensitive cancers.[74,75,76] In addition, studies have shown that flaxseed can reduce estrogen levels through excretion in the urine.[77,78]
On the basis of preliminary data testing flaxseed for its effect on hot flashes and related endpoints,[79,80][Level of evidence: I] an open-label pilot study was conducted to evaluate 40 g of flaxseed in decreasing hot flashes. This study of 30 women showed a 57% reduction in hot flash scores and a 50% reduction in hot flash frequency over a 6-week period.[81] However, a follow-up phase III, randomized, controlled trial conducted by the North Central Cancer Treatment Group with 188 women failed to show any benefit of 410 mg of lignans in a flaxseed bar over placebo.[82][Level of evidence: I]
Many plants and natural products are touted as wonderful remedies for hot flashes. Some of these products are plant phytoestrogens, and some have unknown properties. The agents include dong quai, milk thistle, red clover, licorice, and chaste tree berry. There is incomplete understanding of the biology of these agents and whether taking them would impact breast cancer risk or recurrence in a negative or positive way. Data suggest that these plants have different effects, dependent not only on the dose used but also on a woman's hormone environment when she takes them. Little is known about these agents, and caution with respect to taking them—if a woman is to avoid estrogen supplementation—is needed. [83,84,85,86]
Several pilot trials have evaluated the use of acupuncture to treat hot flashes.[87,88,89,90][Level of evidence: I] Research in acupuncture is difficult, owing to the lack of novel methodology—specifically, the conundrum of what should serve as an adequate control arm. In addition, the philosophy surrounding acupuncture practice is quite individualized, in that two women experiencing hot flashes would not necessarily receive the same treatment. It would be important to study acupuncture utilizing relevant clinical procedures; so far, acceptable research methods to accomplish this are lacking. Therefore, the data with respect to the effect of acupuncture on hot flashes are quite mixed, with many studies suffering from ineffective control arms. Therefore, as concluded in at least one review, there is not a body of evidence to definitively delineate the role or practice of acupuncture for hot flashes.[91] (Refer to the Vasomotor symptoms section in the PDQ summary on Acupuncture for more information.)
Prostate cancer
Data regarding the pathophysiology and management of hot flashes in men with prostate cancer are scant. The limited data that exist suggest that hot flashes are related to changes in sex hormone levels that caused instability in the hypothalamic thermoregulatory center analogous to the proposed mechanism of hot flashes that occur in women. As with women with breast cancer, hot flashes impair the quality of life for men with prostate cancer who are receiving androgen deprivation therapy. The vasodilatory neuropeptide, calcitonin gene–related peptide, may be instrumental in the genesis of hot flashes. With the exception of clonidine, the agents mentioned previously (refer to the Other pharmacologic interventions for hot flashes section of this summary) that have been found effective for hot flashes have shown similar rates of efficacy when studied in men. Treatment modalities include estrogens, progesterone, SSRIs, gabapentin 300 mg 3 times per day as an option for men,[92] and cyproterone acetate, an antiandrogen. The latter is not available in the United States.
One large, multisite study from France [93] randomly assigned men who were taking leuprorelin for prostate cancer to receive venlafaxine, 75 mg; cyproterone acetate (an antiandrogen), 100 mg; or medroxyprogesterone acetate, 20 mg, when they reported at least 14 hot flashes per week. All three treatments significantly reduced hot flashes, with cyproterone resulting in a 100% median reduction, medroxyprogesterone resulting in a 97% reduction, and venlafaxine resulting in a 57% reduction at 8 weeks. More adverse events were reported with cyproterone acetate, including one serious adverse event (dyspnea) attributable to the drug. Venlafaxine was not associated with any serious adverse events and overall had a 20% adverse event rate attributable to the drug. Medroxyprogesterone was the most well tolerated, with an adverse event rate of 12%, but with one serious event, urticaria. The most frequent side effects for all agents were related to gastrointestinal issues: nausea, constipation, diarrhea, and abdominal pain.[93]
Pilot studies of the efficacy of the SSRIs paroxetine and fluvoxamine suggest these drugs decrease the frequency and severity of hot flashes in men with prostate cancer.[94,95] As for women with hormonally sensitive tumors, there are concerns about the effects of hormone use on the outcome of prostate cancer, in addition to other well-described side effects.[96]
Other Pharmacologic Interventions
Clinical experience suggests that the H2 blocker cimetidine may be useful in the management of cancer-associated sweats. Given the vascular action of 5-hydroxytryptamine, somatostatin analogs may play a role in the nonspecific management of sweats. The use of low-dose thioridazine for the management of sweats in advanced cancer is no longer advocated because of reports of torsade de pointes arrhythmias [97] and sudden death.[98]
Effective management strategies for fever and sweats are limited by the paucity of data about symptom epidemiology and contributing pathophysiologies in the advanced cancer patient. Notwithstanding, careful history taking and physical examination can be used to develop a plan for diagnostic evaluation that is consistent with the patient's location in the disease spectrum and goals of care. For some patients, improved quality of life outweighs potential survival advantages. Fever, sweats, and hot flashes detract from quality of life in a significant number of patients with cancer or a history of cancer. Management strategies require an understanding of the underlying causes and pathophysiologic mechanisms, as well as knowledge of the patient's goals of care. Treatment interventions include pharmacologic, physical, dietary, and behavioral modalities.[1]
Check NCI's list of cancer clinical trials for U.S. supportive and palliative care trials about fever, sweats, and hot flashes, neutropenia, hot flashes and hot flashes attenuation that are now accepting participants. The list of trials can be further narrowed by location, drug, intervention, and other criteria.
General information about clinical trials is also available from the NCI Web site.
The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
Editorial changes were made to this summary.
This summary is written and maintained by the PDQ Supportive and Palliative Care Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ NCI's Comprehensive Cancer Database pages.
If you have questions or comments about this summary, please send them to Cancer.gov through the Web site's Contact Form. We can respond only to email messages written in English.
Purpose of This Summary
This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the pathophysiology and treatment of fever, sweats, and hot flashes. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.
Reviewers and Updates
This summary is reviewed regularly and updated as necessary by the PDQ Supportive and Palliative Care Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).
Board members review recently published articles each month to determine whether an article should:
Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.
Any comments or questions about the summary content should be submitted to Cancer.gov through the Web site's Contact Form. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.
Levels of Evidence
Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Supportive and Palliative Care Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
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PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as "NCI's PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary]."
The preferred citation for this PDQ summary is:
National Cancer Institute: PDQ® Fever, Sweats, and Hot Flashes. Bethesda, MD: National Cancer Institute. Date last modified <MM/DD/YYYY>. Available at: http://cancer.gov/cancertopics/pdq/supportivecare/fever/HealthProfessional. Accessed <MM/DD/YYYY>.
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Roeper: Tribute to Roger Ebert's thumbs-up sign
Roger Ebert's famous thumbs-up sign took on a very different symbol as he battled cancer, according to Richard Roeper, who co-hosted At the Movies with Ebert for eight years
Roeper says that after Ebert lost the ability to speak following cancer surgery, he would give the symbol following each visit, especially when in the hospital.
"When you'd leave him, he'd give you a thumbs up," says Roeper. "It was more like a carry on thing. It was business as usual. You wouldn't walk out of the hospital room feeling depressed. You'd walk out of there thinking I wish I had half the enthusiasm that Roger does."
"He was human like the rest of us, there were moments when things were very tough," says Roeper. "But when I saw him at the hospital or a home, there was nothing but passion and enthusiasm."
Ebert died on Thursday at age 70 two days after announcing that he would be forced to cut back from his Pulitzer Prize-winning movie reviewing following his cancer's return. Roeper says he was aware of Ebert's condition, but still "shocked" by the news on Thursday.
"I knew it was not going to get better," says Roeper. "I didn't think (in two days) we were going to lose him. But I feel that once he shared with the world that he was going to step back, maybe he found he had that little bit of closure with his legions of fans and he was able to let go."
Roeper says that when he started work at the Chicago Sun-Times in the late 80s, Ebert was already a long-established television star alongside his famous on-air movie review partner Gene Siskel.
"It was like having our own rock star in the newsroom," says Roeper of working with Ebert. "But he'd be in his comfortable Rockport shoes and a sweater vest. He didn't change. It was the same haircut, the same glasses. He used to tease me about how much I'd spend on my haircuts. He'd tell me he got his for eight bucks at Supercuts. That was the kind of guy he was."
Ebert and Siskel had what Roeper calls a "brotherly, love-hate relationship." They would take their film disagreements to most any other topic.
"Neither one of them wanted to give into the other on anything," says Roeper. "I interviewed them for the 20th anniversary of their show and walking to the elevator they would be arguing about the best sandwich in Los Angeles. It never ended."
Ebert took more of a "proud uncle" role when Roeper took the chair next to Ebert in 2000. The relationship flourished through their last in-person meeting, a few months ago in the hospital.
"The hospital visit quickly turned into a film meeting with Roger, his wife Chaz, and the film editor on the upcoming spring movie schedule, who was going to review what and what we were looking forward to seeing," says Roeper. "It was classic Roger. Nothing melancholy. Just movies and the business at hand."

subset: commoncrawl


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Professor, Department of Cell Biology
Professor, Department of Genetics
The Joseph and Gertrud Buchler Chair in Transgenic Medicine
Faculty Supervisor, Gene Modification, Gene Targeting and Transgenic Facilities
The maintenance of genomic integrity in all organisms requires multiple DNA repair pathways that are involved in the processes of DNA replication, repair and recombination. Perturbations in these pathways can lead to increased mutation rates or chromosomal rearrangements that ultimately result in cancer. MMR is one of the repair systems that mammalian cells employ to maintain the integrity of its genetic information by correcting mutations that occur during erroneous replication. Mutations in MMR genes are linked to one of the most prevalent human cancer syndromes, Lynch syndrome and a significant number of sporadic colorectal cancers. At the molecular level tumors that develop in these patients display increased genomic mutation rates as indicated by increased instability at microsatellite repeat sequences (termed microsatellite instability, MSI). MMR in eukaryotes is complex and involves several homologs of the bacterial MutS and MutL proteins. In mammals, the initiation of the repair process requires two complexes formed by three different MutS homologs (MSH): A complex between MSH2-MSH6 for the recognition of single base mismatches and a complex between MSH2-MSH3 for the recognition of insertion/deletions. The repair reaction also requires a complex between the two MutL homologs MLH1 and PMS2 that interacts with the MSH complexes to activate subsequent repair events which include the excision of the mismatch carrying DNA strand and its re-synthesis. These steps are carried out by exonculeases, polymerases and a number of replication associated proteins. In addition to correcting DNA mismatches, the MMR system mediates an apoptotic response to DNA damage and both of these functions are thought to be important for genome maintenance and tumor suppression. We have generated gene targeted mouse lines with inactivating mutations in all the different MutS and MutL homologs, and also in genes that function in the later MMR steps to study their roles in genome maintenance and tumor suppression. In addition, we have generated knock-in mouse lines with missense mutations and conditional knockout mouse lines that inactivate specific MMR functions and/or model mutations found in humans. Our studies indicate that specific MMR functions play distinct roles in maintaining genome stability and that defects in these functions have important consequences for tumorigenesis. We are currently studying the functions of MMR in intestinal stem cells and cancer stem cells and how loss of MMR in stem cells affects tumorigenesis and the response of tumors to chemotherapeutic treatment. Our studies have also revealed that some of the MMR proteins play essential roles in class switch recombination and somatic hypermutation during antibody maturation and the control of meiotic recombination in mammals.
Selected References:
Wang J.Y.J and Edelmann W. 2006. Mismatch Repair Proteins as Sensors of Alkylation DNA Damage. Cancer Cell. 6:417-418.
Schätzlein S., Ju Z., Stepczynska A., Reddy K., Saal N., Lechel A., Roychoudhury A., Kuhnel F., Schirmacher P., Wei K., Edelmann W. and Rudolph K.L. 2007. Exo1 deletion prevents DNA damage signalling and prolongs lifespan of telomere dysfunctional mice without accelerating cancer formation. Cell. 130:863-877.
Takedo M.M. & Edelmann W. 2009. Mouse models of colorectal cancer. Gastroenterology. 136:780-798. PMID: 19263594
Kucherlapati M.H., Lee K., Nguyen A.A., Clark A.B., Hou H. Jr.,Rosulek A.,Li H., Yang K., Fan K., Lipkin M., Bronson R.T., Jelicks L., Kunkel T.A., Kucherlapati R. and Edelmann W. 2010. An Msh2 Conditional Knockout Mouse for Studying Intestinal Cancer and Testing Anti-cancer Agents. Gastroenterology. 138:993-1002.
van Oers J.M., Roa S., Werling U., Liu Y., Genschel J., Hou H. Jr., Sellers R.S., Modrich P., Scharff M.D., Edelmann W. 2010. PMS2 endonuclease activity has distinct biological functions and is essential for genome maintenance. Proc Natl Acad Sci U S A. 107:13384-13389.
Schaetzlein S., Chahwan R., Roa S., Avdievich E., Wei K., Eoff R.L., Sellers R.S., Clark A.B., Kunkel T.A., Scharff M., Edelmann W. 2013. Mammalian Exo1 encodes both structural and catalytic functions that play distinct roles in important biological processes. Proc Natl Acad Sci U S A. 110:E2470-2479.
van Oers J.M.M., Edwards Y., Chahwan R., Zhang W., Smith C., Pechuan J., Schaetzlein S., Jin B., Wang Y., Bergman A., Scharff M.D., Edelmann W. 2013. The MutSb complex is a modulator of p53-driven tumorigenesis through its functions in both DNA double strand break repair and mismatch repair. Oncogene, in press.
More Information About Dr. Winfried Edelmann
Material in this section is provided by individual faculty members who are solely responsible for its accuracy and content.


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DENISON, TX -- Saturday several people walked the plank right into Lake Texoma.
It was all part of the first annual Pirate Plank Walk. Participants boarded the Compass Rose, a pirate ship docked at Grandpappy Point Marina, and walked the plank in support of our veterans.
All money raised is going to Denison's Veterans of Foreign Wars Soldier Relief Fund -- which helps veterans, widows and their families during times of need. A couple thousand dollars was raised for the veterans.
"And all the money stays here locally and it was just fun way to give back to the community, but more importantly, give back to all the soldiers who have given so much for our country," Tami Odom said.
"If they can go to war, I can jump in some cold water," participant Bobby Defir said.
The Odom's say they plan to make this an annual event.


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Hi guys, we're so happy you stopped by! Thanks to your help we will be able to make Ringbow a reality and revolutionize the way we use our touch devices.
IGN - "definitely worth it"
Robert Scoble - "I want one!"
Mashable - "Ringbow will bridge the gap between touch control and accuracy while gaming"
Pocketgamer - "you should check out the new "next-generation" gaming peripheral"
Engadget - "Ringbow promises directional pad-assisted touch gaming"
Joystiq - "solving the "pesky touchscreen D-pad" crisis"
Geek - "the perfect compliment to touchscreen gaming"
Gizmag - "take the best bits of a computer mouse and a gaming joystick and puts them into one device"
So I guess Ringbow is a ring?
Ringbow is the world's first wearable accessory for touch devices that provides the functionalities of a mouse, keyboard and joystick simultaneously with your touch. Ringbow transforms touch screen gaming, allows remote control of your operating system, applications, music apps and presentation tools, allows you to operate and answer your phone remotely and turns your device into a multi-user or multi-player platform.
Since touch screens are controlled with fingers, a finger-worn tool, specifically a ring, is the natural choice for complementing them. Operating Ringbow with your thumb, in conjunction with using a touch device, enables countless new features and a much more efficient user experience. Ringbow multiplies the functionality of your finger together with allowing amazing simultaneous actions providing powerful capabilities and layers of functionality that are simply not available in today's technologies.
Operating the ring with your thumb while using your finger to touch a device provides powerful capabilities and layers of functionality that are simply not available in today's technologies. Ringbow multiplies the functionality of your finger together with allowing amazing simultaneous actions.
Ringbow lets you free your fingers from your device, leaving your hands available to do whatever you feel like doing: eating a sandwich, drinking a beer, high-fiving your buddy or stroking a puppy. Whatever you'd choose to do with your hands!
Ringbow innovates touch devices' gameplay, offering unique additions to existing mobile games as well as developing new games that couldn't previously be played on touch devices. Ringbow also makes porting consoles games and PC games to mobile devices easier than ever which can be done without affecting and damaging their great experience.
Ringbow in a nutshell;
* the world's first touch-screen gaming accessory
* a comfortable ring that you wear on your finger whilst gaming
* adds layers of functionality to each touch
* acts as a mouse/joystick device to use for gaming
* builds a new platform for existing and new games
AT&T FOUNDRY & RINGBOW - We collaborated with the AT&T Foundry to explore the potential of Ringbow. Take a look at how they envision the Ringbow device - http://www.youtube.com/watch?v=KFJw1ZXFvB0
It simply works
Using Ringbow is extremely easy and staggeringly simple. It is designed to provide natural gaming control, similar to the way we operate our console's controllers. This allows for an intuitive gaming experience and a sense of tactile feedback which greatly enhances the user experience.
Ringbow works on Android, iOS (coming very soon) and supports any Bluetooth enabled device. It works natively with the operating system and with a large variety of existing applications, although our mission is to provide users with brand new cool features. To do that we've partnered with some leading game developers so that Kickstarter supporters will receive a package of exclusive games with their Ringbow. We also hope that you'll use our API to enhance your own apps so we can add them to our games and apps directory.
Ringbow offers a D-pad style controller, communicates via Bluetooth and lasts 5 hours per charge. The Ringbow box includes:
- The Ringbow game-ring accessory device
- Micro-USB cable for charging
- Ringbow control panel application for Android & iOS devices
- Game package (see below) including games that were especially designed to support Ringbow, native control of the operating systems and a list of many games that naturally supports Ringbow and works automatically.
- Developers kit includes the Ringbow APIs and plug-ins, technical support, creative guidelines and 24 hours assistance from our team.
We plan on shipping the product in time for the holiday season.
This very first Ringbow model is described as a gaming accessory but it can do much, much more. You can use Ringbow for remote browsing while reading; to correct misspelled emails; to act as a remote control for your TV; to answer phone calls while driving; to transform your tablet into a gaming console for your kids;
Back us and you'll be among the first to get your hands (or should we say fingers!) on a Ringbow
For the last 2 years we have been researching the concept of Ringbow and developing the product. We've built a number of working prototypes in a variety of ergonomic designs, conducted an impressive commercial pilot with AT&T and recently completed the final Ringbow design and we are now ready to manufacture it for the masses! Prospective partners, distributers and users have recognized Ringbow's great potential, but in order to take the product to the market we need your help.
Your support will allow us to establish a production line, manufacture the product and expand our games and applications offering so that Ringbow users will enjoy a new and exclusive experience.
The funding goal represents the costs of tooling, plastic molds, product certifications and additional software development.
We hope you find Ringbow a powerful and creative tool and hope that you choose to support it. We appreciate your help in spreading the word. Thank you!
Engadget demo: http://www.engadget.com/2011/09/15/atandt-foundry-innovation-center-opens-its-doors-in-palo-alto-to-h/
Old garage-made movies that helped us explain the Ringbow concept:
http://youtu.be/tsqiQb_F5Gs , http://youtu.be/8PkiOj2MZGA
Selected to present at Futur En Seine, 2012
Chosen as Microsoft's 'Think Next's' top 20 Leading Technologies of the FutureWinner of 2010 Mobile Monday Peer Award for "future potential"
Ringbow Gaming Package
All of our backers will receive the Ringbow Gaming Package which includes games designed specifically for the Ringbow functionality, and special editions of games that have been enhanced by Ringbow thanks to the special features of our device. The Ringbow Gaming Package includes so far:
- Vector Runner Ringbow Blast: The highly popular Vector Runner by Littlegrey Media receives a boost with the new Ringbow features that introduce new skills for your runner, such as jumping, shielding and bonus combos available only in this Ringbow version.
- Elastic Ocean: From Sebastian Janisz, a.k.a. Ultimate Walrus, the developer of featured indie games like Lackadaisium and Snake 2 comes this amazing action-adventure game with an incredible variety of new game mechanics to explore.
Play as Lil' Winston the tiny deep sea diver, graduated from SDA (Stretchy Diver Academy). It's time to prove yourself by plunging into the depths of the ocean on a four-year search for sunken treasure. Bring back something valuable and maybe you'll prove to everyone once and for all that you can be a Stretchy Diver if you want to!
- Ringboy: Jock is in love with Myra, the prom queen, and rudely kidnaps her. Albert, also known as Ringboy, sets off with his magical ring to save the prom queen and become her prom king.
Control Ringboy with your Ringbow while touching everything to solve puzzles and test your reflexes. Completely interact with the wonderful environments that make up the Ringboy world.
- Kingdom Elemental: The Ringbow Wars: From Chronic Logic comes the new episode in this action-packed strategy game, where you can finally enjoy full control of the battlefield on your touch screen device. Issue advance commands and enjoy special weapons and powers with the Ringbow supreme gameplay.
Game details may vary throughout the campaign, as we are working diligently on bringing you more games and including them in our free launch package for Kickstarter backers only.
Funding period
- (38 days)


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National Register of Historic Places Program
Weekly Highlight: Steel Development House No. 2
Riverside County, California
The National Register of Historic Places is the official list of the Nation's historic places worthy of preservation. Authorized by the National Historic Preservation Act of 1966, the National Park Service's National Register of Historic Places is part of a national program to coordinate and support public and private efforts to identify, evaluate, and protect America's historic and archeological resources.
Steel Development House Number 2 is one of seven all-steel
homes-all clustered in the same neighborhood-created by the
architectural team of Donald Wexler and Ric Harrison, the structural
engineer Bernard Perlin, and the builder Alexander Construction
Company. The house is primarily composed of steel and glass
on a concrete foundation with no structural wood and represents
a unique synthesis of off-site prefabrication and on-site assembly.
The house exemplifies simple yet elegant concepts in midcentury
modern design plus the novel use of steel construction, demonstrating
the possibilities for rapidly-assembled and affordable homes
for the middle class that were designed to withstand the harsh
desert environment. The property has excellent integrity in
all aspects, and appears much as it did as built.
Read the full file on the Steel Development House No. 2.
To see more photographs of National Register properties go to our photostream on Flickr.
See our Weekly List (with previous highlights)


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Policy and Procedures
Since 1983 Williamsburg Regional Library has hosted displays and art exhibits in the Williamsburg Library Gallery, a portion of the library that doubles as the lobby of the Williamsburg Library Theatre.
The Gallery consists of approximately 80 linear feet of lighted walls and two glass display cases.
Library Displays policy:
"Williamsburg Regional Library displays are used to promote materials, services, and/or events. Staff members select the topics, materials, locations, and dates for displays."
[Approved by WRL Board of Trustees October 1994. Approved as amended by WRL Board of Trustees June 26, 2002. Approved as amended by WRL Board of Trustees September 29, 2004. Reaffirmed by WRL Board of Trustees January 23, 2008. Reaffirmed by WRL Board of Trustees May 25, 2011. Reaffirmed by WRL Board of Trustees May 27, 2015, Approved as amended June 27, 2018]
Information for Artists:
Williamsburg Regional Library invites artists to apply to display their artwork at the Williamsburg Library, 515 Scotland St. While the library usually has a waiting list of approximately one year for exhibits, you can submit an application online or download an application form to exhibit at any time. If your work is accepted to display, you will be notified about the time periods that are available. Exhibit times range from 4 to 8 weeks.
Because of the nature of the exhibition area as a gathering space and one of three entrances to the library, the Gallery is unable to accommodate freestanding artwork. The art must also be suitable for view by the broad community of people who visit the public library.
Generally the library accepts individual artists who have a sufficient body of work to fill the Gallery space. Classes or assemblages of artists are also invited to submit as a group. Periodically the library will also organize open exhibits that will allow unrelated artist to exhibit their work.
Items chosen for display must be mounted or framed and have either wires or hooks on the back that will allow them to be hung on the wall. Library staff will provide nails for hanging and assistance in hanging the works. Works displayed must weigh less than 25 pounds.
Works exhibited should be identified with the name of the artist, title (if any), and either a price or "NFS" (Not For Sale) indicated on the label. Labels should be typed and not exceed business card (2" x 3 ½") size so that they can fit in plastic holders that the library will provide. A letter-sized artist statement or exhibit title panel should also be provided the artist(s).
Works exhibited may be available for sale by the artist. In those cases the artist will provide contact information as part of the artist statement or title panel so that prospective purchasers can contact the artist directly. The library does not take any percentage of the sale.
The library will promote the exhibit through its normal public information channels. The library will also make available a three-hour block of time where the artist or artists can host an opening reception that is open to the public.


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The peak viewing audience was 3.1m at 10.30pm.
O'Sullivan was of the view afterwards that the final should be best of 13 frames to ensure an earlier finish but, actually, what needs to happen is an earlier start.
The snooker drew a 13% share to BBC2, which was the most watched channel after 10.30pm.
The final also beat Match of the Day 2 on BBC1, which drew an audience of 2.2m, and Channel 4's Celebrity Big Brother, which pulled in 2.3m.
31 comments:
- Isak said...
I agree, it's ridiculous to start the final session at 9 pm! They should change it to around 7 pm in my opinion. Is there a reason to have the final so late or is that just "the way it's always been"?
- 3:59 pm
The final started at 8pm but yes that's still too late. Great final and will have done snooker the world of good, especially, if we're honest, with Ronnie winning it.
Never seen him look so pleased.
- 4:19 pm
- Isak said...
Oh sorry, 8 pm GMT... Where I'm located that's 9 pm ;)
To be honest I cheered for Selby... Let's hope he wants revenge in the Crucible!
- 4:25 pm
O'Sullivan was of the view it should be best of 13 frames. Well bully for him. Good job he's not in charge although it sounds like he thinks he is.
Of course earlier session start times are the answer, not shorter finals. If anything, all matches should be longer in order that the better player comes out on top more frequently.
- 4:26 pm
Lest get some things straight here, Ronnie doesn't say incredibly clever things which we should all listen carefully to.
Most of what Ronnie says contradicts what he has said previously.
He is a great player, the best I have seen, yet last night was one of those occasions where the best player didn't win.
Selby threw frames away and Ronnie took full advantage although I would concede that to win The Masters with what amounts to a strange cue is an unbelievable feat.
Good tournament and great news about viewing figures.
Up yours Patrick Collins.
- 4:35 pm
I'm sorry, I think the best player clearly did win.
- 4:45 pm
According to some of the papers, snooker is dead. There where 3.1 million viewers watching the final in the UK alone. The snooker drew a 13% share to BBC2, which was the most watched channel after 10.30pm. The final also beat Match of the Day 2 on BBC1, which drew an audience of 2.2m, and Channel 4's Celebrity Big Brother, which pulled in 2.3m. So, snooker seems to be dying? yeah, right.
- 4:48 pm
The session times should definitely be changed, it's ridiculous the finish to these final's. I had to get up for work just after 4am so obviously i missed out on Ronnie's win which is a shame because i had been watching the quality play at the masters all week.
It seem's to be the norm now for late late finishes, Murphy won the uk championship at 00.20 and lest we forget Higgins win in the world final over Selby which run very late and that was 18-13, it would have been at least 3-4 in the morning if that had gone all the way. Dott beating Ebdon in the world final was also a late finish.
It's not just the watching tv audience, what about the people at the game? i'm sure the underground station would have been closed at that time of morning.
For me it should be 1.30pm start and the evening session at 6.30 or 7pm start that way their shouldn't be so late finishes and also we might get more column inches about this great sport in the press and that the youngsters get to see the conclusion aswell, you never know, they might talk about the snooker rather than the football football football that they do now.
- 4:54 pm
RIch P said...
The final started at 8pm but yes that's still too late. Great final and will have done snooker the world of good, especially, if we're honest, with Ronnie winning it.
Never seen him look so pleased.
i I am honest id rather Selby won it, for his potential, professionalism and for snookers future.
i dont know who the WE is in your statement. perhaps the majority, but certainly nowhere near exclusive.
loads of folk cant stand ronnie, even though they admit he plays amazing snooker.
great viewing figures. was the venue sold out?
- 5:51 pm
- jamie said...
Strong figures about the same as last year when Selby walked it. The game is not dead but I would like to see music walk ons. This is some song choices.
Ronnie O'Sullivan- Either Rocket Man by Elton John or Can't Get No Satisfaction by The Rolling Stones.
Stephen Maguire- Fire by Arthur Lee
Marco Fu- No Emotion by Idlewild or Kung Fu by Ash
Neil Robertson- Australia- Manic Street Preachers
Ali Carter- El Capitan-Idlewild
Ryan Day- Perfect Day- Lou Reed
Peter Ebdon- Come On- The Verve
Stephen Hendry- Smile- Lily Allen
- 5:56 pm
There's far too much gibberish being spouted, about "speeding up the game". How many classic best of 17 or best of 19 (or more) finals have there been? Plenty. How many memorable "best of 13", 30 second shot clock finals have there been? None.
- 7:03 pm
It has been said for years that starting finals nights at 8pm is too late but bbc (so we have been told) set the timings. Common sense will not prevail because bbc makes the decision on this and puts its own scheduling ahead of the best interests of the sport and the viewing public. World Snooker is obviously happy to go along with this to keep bbc happy. If snooker is 'dead' and pulling in better viewing figures than match of the day does that mean that football is 'dead' too?
John H
- 7:30 pm
So a snooker final won a ratings war when two of the current most popular players were battling out an epic final against each other? Big deal.
Just think about what happened when lesser 'Gods of the Baize' would have gotten this far...
I don't think snooker is as dead as O'Sullivan seems to claim, but to say it's very much alive isn't really true either. They could do with a little boost (although I doubt Cowell or darts like dressing up (it would be hilarious for one time only, though. For a thing like Sport Relief) will help)
- 10:12 pm
Can you put brackets inside brackets?
- 11:15 pm
- SupremeSnooker said...
Some bright sparks at the BBC will probably use these healthy ratings figures as proof that snooker has reached a "new audience" by dropping Clive Everton.
I don't especially dislike any commentators, but most snooker fans I've spoken to in the last few days MUCH preferred having Clive as part of the team, and I have to say I strongly agree.
- 2:32 am
id be surprised if many fans noticed much difference, unless they normally watch every session of every match, and remember back every masters tournament. he didnt do every session of every match before, so unless you tune in to more than half the matches theres as much chance of listening to him as not, until this year, so how someone, or lots of people can have missed one commentator so badly is beyond me.....yeah i know im setting myself up for the childish ones on here to reply rubbish *at* me
- 7:29 am
On the subject of commentators i wish they'd use Neal Foulds other for than the World Championships because he's a good commentator.
- 8:08 am
It was a closely contested final, an exciting fight with twists and turns, therefore the largest part of the audience stayed tuned. Also, Ronnie and Mark are the two biggest box office attractions, hence the remarkable viewing figures. Be realistic, these figures would be substantially lower in almost any other case. No serious conclusions can be drawn from these numbers on the general state of snooker, which may or may not be in decline - to be honest, I don't know.
As for the starting times, we are more affected here, in continental Europe. The final ended around 1.15am here.
Who was the better player? All I can say that yesterday I watched the final again, and I am still surprised that Mark managed to throw this away. And even more surprised that this time Ronnie was, somewhat uncharacteristically, the greater fighter.
- 10:01 am
What is that phrase about lies, damn lies and statistics?
I think putting snooker up against Match of the Day 2 which featured the fare served up Fulham, West Ham, Spurs and Portsmouth means that the former was always going to win.
What is that phrase about straws and clutching?
- 10:30 am
Ronnie's strange statement about "dying snooker" definitely seems to revitalize the interest to the sport. I don't remember such amount of articles and opinions during last five years.... probably, only about his press-conference in China? Yes, that's right. Nowadays Ronnie is a biggest showman in snooker.
- 11:06 am
Ronnie said that the sport is dying, not that it is dead. If you are bleeding, you also are not dead, are you?
Such is the state of snooker in the UK and Ireland. It's diminishing, bleeding, dying.
There's some rising interest in continental europe and appearently quite a boom in china. Although I don't think that there could be found a sponsor who pumps 200k in a maintour event in Germany. However, every professional snooker tournament in Germany or Austria will have a packed house.
There's quite a small, but extremely enthusiastic fanbase in the german speaking contries. That leads me to a question. Dave H, do you know the rating figures of Eurosport for the final? I can't quite find something about it, but it is said that alone German Eurosport draws 1m on special snooker occasions. So the ratings throughout Europe could well match the ones on the BBC.
I think the main interest of World Snooker should be to promote World Snooker, not Snooker on the British Islands. You have the WSC, the UKC, the Grand Prix and the Masters in Britain. They are the heart of professional Snooker. But you should give other tournaments to other countries. Smaller ones to start with, in some high profile locations. The Tempodrom in Berlin for example, where there could be an enthusiastic 2000+ crowd for nearly every session. That would give the german speaking countries (where their live nerly 100 000 000 people) the boost they need in terms of snooker. And I don't think that travelling to Germany would be such a big deal. If there was a succesful tournament, that could really attract new sponsors.
The problem is that World Snooker is aiming to please the BBC, and the BBC just thinks about the BBC. Snooker is only dying on BBC, whereas elsewhere there would be foundations to build on. If World Snooker doesn't react quickly, Snooker will be dead in Britain and be aborted in other regions.
To push the analogy: Don't conduct euthanasia for Snooker in Britain and abortion for Snooker in the rest of the world at the same time!
- 11:15 am
I think the last post sums it up perfectly. Snooker received so much press exposure and that's down to one man and one man only - Ronnie O'Sullivan. Without Ronnie, snooker really would be dying. Audience figures were boosted because he was there.
Not sure about Selby being big box office as a O'Sullivan - Williams or O'Sullivan - Higgins final would have been a bigger draw.
The reality is snooker is Ronnie. I heard Selby doing an interview on Chris Evans' radio two show before the tournament. Mr Charisma - not, certainly did nothing to sell the tournament.
Yes, Ronnie comes out with some odd things but this gets the column inches at the end of the day.
I do wish Barry Hearn would become move involved in things though as he seems to have the Midas touch. Another thing - maybe another tournament in central London wouldn't go amiss.
- 11:23 am
My post was refering to the previous post by the way!
- 11:23 am
A ranking tournament in London would be great, it seems crazy that there isn't one to be honest.
- 11:37 am
Am glad the figures were good. Am I the only one who thinks the final could start earlier and the TV could catch up? Either that or abolish intervals which waste lots of time. When there are long spells of live coverage you often end up with a certain amount of dross (I admit this didn't really happen in the final apart from the re-racks). Or even if the last session of the final is live, couldn't some of the coverage during the week have been deferred to avoid programmes not getting results or - as often happens on the 7pm show - getting one tactical frame and then going off air with highlights to follow much too late - 11.20 or later. If people are really into long runs of live coverage they can use the Red Button or Eurosport anyway.
- 11:50 am
- andy said...
It didn't start at 8pm where I lived, ....9pm, I was knackered Monday morning, so much so I decided to not bother with work until the afternoon!!!!
I'm amazed the final beat MOTD 2 in the ratings, ...good news for snooker for a change! :oD
- 1:23 pm
In response to a couple of comments...
"So a snooker final won a ratings war when two of the current most popular players were battling out an epic final against each other? Big deal.
Just think about what happened when lesser 'Gods of the Baize' would have gotten this far."
Actually, the figures were much the same last year for Selby v Lee, and as recently as 2005 there were EIGHT MILLION watching the Murphy v Stevens final in Sheffield.
Within recent years, there was also a second round match between Marco Fu and Alan McManus in Sheffield which attracted more than 3 million.
So while O'Sullivan is a great drawing card, let's not start buying into the notion that the game depends on him to get good ratings.
"I think putting snooker up against Match of the Day 2 which featured the fare served up Fulham, West Ham, Spurs and Portsmouth means that the former was always going to win."
Don't know what this is about at all. There was very big interest in the Tottenham/Portsmouth match because of Redknapp, Defoe, the fact that both teams have been struggling for form etc..
Don't forget that even the most anonymous Premier League football match gets more media coverage than just about any snooker match, so it's significant to see snooker beating PL footy at any time.
And also, when the live screening of the 2002 FA Cup final between Arsenal and Chelsea went up against the World Championship, it was the snooker which got bigger ratings. And it wasn't even the final.
- 1:23 pm
Yes, and trying to talk down the quality of the matches on MOTD2 overlooks the fact that the snooker also beat everything else that was on at that time.
Shaun Murphy made an interesting point during the week about changing viewing tastes, saying that people now seem more interested in watching people cracking up on Big Brother than watching talented snooker players doing their thing.
I think it was a very good point, but isn't it interesting that the week then ended with Big Brother being beaten in the ratings by the snooker?
- 1:27 pm
Whoever said;
"Don't know what this is about at all. There was very big interest in the Tottenham/Portsmouth match because of Redknapp, Defoe, the fact that both teams have been struggling for form etc.."
All the 'big' teams had played on the Sunday. Sorry, Redknapp and Defoe means nothing compared to what the top teams were doing.
"Don't forget that even the most anonymous Premier League football match gets more media coverage than just about any snooker match, so it's significant to see snooker beating PL footy at any time."
Something to do with earlier kick-offs and finishing times, which you can set your watch by - completely the opposite of snooker.
And as for; "And also, when the live screening of the 2002 FA Cup final between Arsenal and Chelsea went up against the World Championship, it was the snooker which got bigger ratings. And it wasn't even the final."
Two London clubs. And the rest of the land ain't really bothered. Nice to see though you are using really up to date info. 2002! Or do you have nothing else up-to-date to hand?
- 2:30 pm
Why do people like the last person who posted even bother coming on here?
They just seem to want to be negative about any good thing that happens for snooker.
If a snooker match ends up getting more viewers than all the other programmes on at the same time, that's great for the game.
Making daft assertions about nobody outside London being "really bothered" about the FA Cup final, and trying to talk down the footy fare being offered on the other side, won't change that.
This is the sort of flippant, illogical negativity which does so much damage to the game. I don't understand why anyone claiming to be a snooker fan would want to join in with that.
- 5:55 pm
Perhaps they are snooker fans waiting for, as you put it, "any good thing that happens for snooker."
The Masters was a good final. It did though finish far too late, and, the tournament itself was played out without a sponsor being in place.
That is what is damaging snooker, not what someone, flippant or otherwise, posts on here.
Or are you happy with how things are in the world of snooker?
- 2:15 am


text:
Maybe U.S. public schools don't stink
The drumbeat is hard to miss: Our schools are failing. Public education is in crisis. Our students are falling further and further behind.
The rhetoric comes from the left and right, from educators and politicians and lobbyists and CEOs and even Education Secretary Arne Duncan. The deep dysfunction of our public schools is said to threaten not only America's economy but also its national security.
Story Continued Below
But a vocal group of contrarians is challenging that conventional wisdom. The latest weapon in their arsenal: A new book out this week by education historian Diane Ravitch, who argues that the biggest crisis facing public education is the relentless message that public education is in crisis.
( Sign up for POLITICO's Morning Education)
It's a debate with broad power to shape the nation's $600-billion-a-year investment in public education. Where's the truth? That's not always easy to discern. Here's a look at four key talking points — and the facts (and spin) behind them.
1. China is eating us for lunch
A new video about the failures of public schools making the rounds on social media starts by introducing viewers to "the most important number in all of education…32!"
Why 32?
Well, that's where the U.S. came out in the PISA international math test, given to 15-year-olds around the world in 2009. Only 32 percent of American kids scored proficient, which put us at 32nd in the world, miles behind perennial powerhouses like Shanghai, Singapore, Hong Kong and Korea — and also far behind nations less frequently thought of as academic superstars, including Estonia, Iceland and Slovenia.
( Also on POLITICO: The Common Core money war)
Sounds grim. And Harvard education professor Paul Peterson argues that it is. "If we're 32nd in the world, that's a pretty serious matter," said Peterson, a co-author of the new book " Endangering Prosperity: A Global View of the American School," which the video was produced to promote.
Then again, we're 32nd on just one test. American kids do better relative to the world — though they're still far from elite — on the PISA science and reading exams.
And they do better as well on a different, equally respected, international math test known as TIMSS.
On the most recent TIMSS test, from 2011, American eighth-graders handily outscored seven nations that had the edge on the U.S. in the 2009 PISA exam, including Great Britain, Australia — and, yes, Slovenia. Fourth-graders rocked the TIMSS test even more: They came out ahead of a dozen countries that had beaten the U.S. on the PISA exam.
( Also on POLITICO: Online courses don't live up to hype)
As for China, it doesn't participate as an entire nation; only students from three relatively wealthy regions — Shanghai, Macao and Hong Kong — are tested. That's important to note because income correlates with success on standardized tests. Finland, often at the top of the global rankings, has a child poverty rate of just 5 percent. In the U.S., it's 23 percent.
One more point: Any test contains sampling error, so the precision of global rankings is an illusion. On the 2009 PISA reading assessment, for instance, the U.S. officially ranked 15th among the 34 member nations of the Organisation for Economic Co-operation and Development, which sponsors the exam. But an OECD official told POLITICO that the U.S. might actually have been as high as 8th — or as low as 20th.
2. Our kids can't do math and that's killing our economy
In her new book " Reign of Error," Ravitch notes that the U.S. has done poorly on every international math test since the first one was given in the mid-1960s.
The low rankings don't concern Ravitch. Bad test scores, she points out, haven't stopped the U.S. from driving major scientific advances decade after decade. American innovation has been so impressive that China's ministry of education is pushing its schools to stop fixating on standardized tests and embrace a more hands-on model of education — the American model.
"The whole thing about being first in the world is nonsense," Ravitch said. "I don't think we should worry that much about Singapore taking over the world."
Peterson, though, does worry — a great deal. He and his co-authors calculate that if the U.S. could just boost its math scores to the level Canada attained on the 2009 PISA test, our economy would grow stronger over the coming decades. How much stronger? The average income of every worker in the U.S. would be 20 percent higher than if we continued to languish at No. 32 in the world rankings, Peterson said. And that's achievable just by matching middle-of-the-pack Canada.
"You would think that would be a reasonable goal to have," Peterson said.
In Peterson's view, it's irresponsible to argue that international rankings don't matter. Sooner or later — and he's betting sooner — poor math scores will catch up to us, he said, as they signal the population is not well-equipped for the jobs of the future. He's particularly concerned that just 7 percent of U.S. students (including just 12 percent of students with college-educated parents) scored "advanced" on the PISA math test, compared with 44 percent of students in Shanghai, 30 percent in Singapore and nearly 14 percent in Canada.
The greatest job growth in the U.S. over the next decade is likely to be in service jobs that don't require advanced math or science, according to the Bureau of Labor Statistics. But those are low-paying jobs. The most lucrative high-growth professions will require strong math and science skills — think software developer, optometrist, bioengineer, veterinarian.
3. We're spending more, but schools are getting worse
Warnings on this theme are generally accompanied by graphs showing steep growth in per-pupil spending — juxtaposed against a flat line representing academic achievement.
That's misleading, however, on two fronts.


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