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(Author's Note: Originally written Jan 5, 2010 – but even more true today.)
CES has descended upon the psyche of the tech world so that it dominates most reports and tweets and attention.
We all wait with bated breath for the declared best new product, most innovative game, most outrageous consumer electronic gadget. We are, in effect, like kids with our noses up against the window pane of the biggest toy store in the world.
I should say that the hyper cool nature of CES is a fairly recent phenomenon. Back when I worked at AT&T, CES was an annual ritual that, frankly, rather inconveniently put a crimp on holiday festivities since many of us had to go the Las Vegas a week before to setup. There went New Year's plans *sigh*. Sure it was fun to see what ingenious gadget was coming into the market, but make no mistake about it; CES was a serious B2B trade show where manufacturers worked hard to woo retailers into carrying their stuff. While there was some consumer coverage, mostly it was confined to the B2B press.
Then, somewhere in the last 4 years, I think driven by the gaming industry, Google, Apple and social media, it took on the glamour of the Oscars for tech set. If a product was even mentioned in a "from CES" report, that was cause for celebration ("I am so honored even to be nominated" kind of thing). CES went from being a B2B event to the event that plays itself out directly to consumers. That shift, in effect, caused CES to become the biggest consumer trade event of all time – even if every consumer is attending by proxy via social media.
But there's more to it than that because at the current level of consumer exposure to the show, CES has transcended the trade show segment and was elevated to become a premier consumer media buy, kinda like SuperBowl. Think about with me. A media buy in SuperBowl was a strategy companies used to catapult themselves – think GoDaddy. This media buy cost a few million bucks, but if played right – you were made. I think CES has taken on that same level of media potential if you account for all the primary, secondary and tertiary coverage that live streaming and social media provide. And instead of a few thirty second spots, you get three days to strut your stuff. Make no mistake about – doing CES right is a multi-million affair. But the pay-off could be huge. In fact, it would not shock me if I learned that CES exceeded SuperBowl in the number of impressions delivered.
That's awe inspiring. Never before has a trade show had that kind of reach and coverage. It seems cosmically fitting that new technology, e.g. social media, would elevate the very essence of CES itself.
Welcome to the year of living intelligently with technology.
Judy Shapiro
Filed under: Communications, Consumer Electronics, Technology | Tagged: advertising, advertising agencies, brand awareness, CES, consumer tech, Judy Consumer, judy shapiro, media planning | 1 Comment »

subset: commoncrawl


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DENVER - First, Andre Iguodala threw a bad pass. Then, he took too many steps.
Two costly turnovers late in a close game. In his Denver home debut, no less.
Miffed by his miscues, Iguodala went to work, scoring six of his 17 points over the final three minutes to help the Denver Nuggets hold off the Detroit Pistons 109-97 on Tuesday night.
"When I make a mistake, I really want to make it up," Iguodala said.
And make it up he certainly did as he played a big role in the Nuggets snapping a three-game skid.
Even before tipoff, Iguodala got the capacity crowd riled up by grabbing the microphone and giving an impassioned speech to the fans: "This is a big year for us! We need your support!"
Then, he came through at crunch time. Not just with his offensive exploits, either, but his defensive intensity as well. He also added 10 rebounds.
"He was a presence everywhere, on every part of the court," Danilo Gallinari said. "He's great for us when he plays like that."
The Nuggets broke out their new canary yellow uniforms for their home opener and played pretty snazzy, especially late in the third quarter when they began opening up a 17-point lead. The Pistons rallied in the final quarter, before Iguodala closed the door with two baskets and a pair of free throws.
Greg Monroe scored 27 points and 10 rebounds for the Pistons, who dropped their fourth straight. Detroit and Washington (0-2) are the only winless teams left in the NBA this season.
"We showed a lot of fight," Monroe said. "We have to push through. At that point, three minutes left, seven-point game, that's definitely a winnable game. We have to find a way to win tight games like that."
Early in the fourth, Iguodala and Corey Brewer hit back-to-back 3-pointers to give the Nuggets a 96-80 lead. Moments later, JaVale McGee brought the crowd to its feet with a thunderous dunk off a lob from Andre Miller.
The Nuggets appeared to be cruising to the win with 7:41 remaining, but the Pistons made things interesting when Jonas Jerebko stole the ball from Iguodala and went in for the dunk.
Iguodala turned the ball over again when he couldn't find anyone to pass the ball to and travelled.
Then, he began his scoring spree, leading coach George Karl to quip after the game that he would be all right with Iguodala doing that all the time, earlier in the game even.
But Karl understands why Iguodala is slowly integrating his way into the offence. It's just his style.
"He's not going to shake the boat," Karl said. "He's going to figure out how we like to play, and figure out what's a good shot and what's not a good shot."
McGee finished with 16 points while Ty Lawson and Kenneth Faried each added 15.
The Pistons played their third of a winding six-game road swing. They return to California on Wednesday night to play Sacramento, before going to Oklahoma City and finishing up in Houston.
Rodney Stuckey came into the game in a shooting funk, hitting just 1 of his last 23 jumpers. But he found his range against the Nuggets as he finished with 17 points.
"He will always be a big part of our success," Monroe said. "We need him to play like he did tonight, attacking the goal, getting to the free throw line. It was good to see that."
Like Stuckey, Gallinari was struggling with his form. He spent nearly 90 minutes after Monday's practice going through shooting drills designed to restore his confidence. He had it going early, but fell off as the young Italian forward had eight points on 3 of 11 shooting.
The Nuggets led by as many as 10 points in the first half, but could never pull away from the pesky Pistons. Kenneth Faried scored 12 points in the first half to send Denver into the locker room with a 58-51 lead at intermission.
Pistons coach Lawrence Frank said he's trying to get his team to buy into the concept of being more unselfish.
"All the best teams are," Frank said. "Look, who's the most coachable player on the Spurs? Tim Duncan. Who's the most coachable player on the Celtics? Kevin Garnett. Who's the most coachable player in Oklahoma City? Kevin Durant. Who's most coachable player of the Miami Heat? LeBron James. This is not calculus. This is not trying to figure out the next Pythagorean theorem.
"This is easy: Your players have to unite and inspire by how they play. It's that simple."
Notes: Pistons F Corey Maggette sat out a fourth straight game with a strained left calf. ... The Pistons were 6 of 12 from behind the 3-point line. ... Former Nuggets F LaPhonso Ellis brought out the game ball before tipoff. ... The Nuggets avoided their first 0-4 start since 1998. ... Denver outrebounded the Pistons 21-8 on the offensive glass.


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Ingrid Chung - Goldman Sachs - Analyst
"Going back to DIRECTV, we've gotten a couple of questions from the audience regarding the equity collar and how that plays out?
Greg Maffei - Liberty Media Corporation - President, CEO
Yes. So the history is LMDIA, Liberty went and bought a whole bunch of incremental shares, about 79 million using a collar and a borrowing. So we borrowed the money from a financial intermediary who collared the stock and then lent us the money to buy the 79 million shares against the puts out of the collar. The stock is about flat, maybe up a little from where we struck the collar so it's not a plus or minus at the moment. It's not — the collar's probably about where it was struck. Neither in the money, nor a cost to the Company. It has effectively a change of controls, so upon the closing of the DTV merger, it could be called by the intermediary. We're in discussions with the intermediary who may want to change the terms of the collar or the rates. It's very low right now. It's paying about LIBOR plus 25. Because effectively the institution is borrowing from itself, given that they wrote the put, they're lending us the money against the puts out of the collar. It's a very low cost loan which is why we liked it. One of the things that's just occurred is that DIRECTV has gone out and done a $2 billion bond issue very successfully, about 225 over LIBOR, Treasury's very attractive issue that will give them the flexibility, they're refinancing some of their existing debt, about $900 million being called and give them the flexibility to pay the collar off or not depending on what the terms the intermediary offers. DIRECTV has the flexibility to do either.
Hopefully we'll reach a successful accommodation with the financial intermediary. But again, we're not beholden to that. In the event that the collar gets unwound, which eventually it will be unwound as the loan matures, that will cause upward pressure on the stock because it's a net short position and unwinding it will cause upward pressure on the stock."


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ANSI Code: CCMT3252MF
Type: CVD-Coated Carbide
Coating: TiN, TiCN, TiC
Composition: A tough cobalt-enriched substrate with a multilayered CVD coating.
Application: KU30T is a new grade designed specifically for the job shop industry where a wide range of workpiece materials is employed. With its tough cobalt-enriched substrate, KU30T performs very effectively in roughing and medium machining operations. The post-coat grinding of the insert permits stable insert seating while the post-coat treatment resists workpiece build-up and microchipping. For roughing steels, cast irons, and stainless steels, your first choices are the RN, -MN, and the RP geometries. For medium machining (and finishing), the MP geometry with a positive rake is suggested.


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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.
Incidence and Mortality
Note: Estimated new cases and deaths from brain and other nervous system tumors in the United States in 2012:[1]
Brain tumors account for 85% to 90% of all primary central nervous system (CNS) tumors.[2] Available registry data from the Surveillance, Epidemiology, and End Results (SEER) database for 2007 indicate that the combined incidence of primary invasive CNS tumors in the United States is 6.36 per 100,000 persons per year with an estimated mortality of 4.22 per 100,000 persons per year.[3] Worldwide, approximately 238,000 new cases of brain and other CNS tumors were diagnosed in the year 2008, with an estimated 175,000 deaths.[4] In general, the incidence of primary brain tumors is higher in whites than in blacks, and mortality is higher in males than in females.[2]
Few definitive observations on environmental or occupational causes of primary CNS tumors have been made.[2] Exposure to vinyl chloride may predispose to the development of glioma. Epstein-Barr virus infection has been implicated in the etiology of primary CNS lymphoma. Transplant recipients and patients with the acquired immunodeficiency syndrome have substantially increased risks for primary CNS lymphoma.[2,5] (Refer to the PDQ summary on Primary CNS Lymphoma Treatment for more information.)
Disease Overview
The glial cell tumors, anaplastic astrocytoma and glioblastoma, account for approximately 38% of primary brain tumors. Since anaplastic astrocytomas only represent less than 10% of all CNS gliomas, phase III randomized trials restricted to the anaplastic astrocytomas are not practical. However, since they are aggressive and often included in studies along with glioblastomas, they are generally managed the same way as glioblastomas. Meningiomas and other mesenchymal tumors account for approximately 27% of primary brain tumors.[2]
Other less-common primary brain tumors include the following in decreasing order of frequency:
Schwannomas, meningiomas, and ependymomas account for up to 79% of primary spinal tumors. Other less common primary spinal tumors include sarcomas, astrocytomas, vascular tumors, and chordomas, in decreasing order of frequency. The familial tumor syndromes (and respective chromosomal abnormalities that are associated with CNS neoplasms) include neurofibromatosis type I (17q11), neurofibromatosis type II (22q12), von Hippel-Lindau disease (3p25-26), tuberous sclerosis (9q34, 16p13), Li-Fraumeni syndrome (17p13), Turcot syndrome type 1 (3p21, 7p22), Turcot syndrome type 2 (5q21), and nevoid basal cell carcinoma syndrome (9q22.3).[6,7]
Clinical Presentation
The clinical presentation of various brain tumors is best appreciated by considering the relationship of signs and symptoms to anatomy.[2] General signs and symptoms include the following:
Whether primary, metastatic, malignant, or benign, brain tumors must be differentiated from other space-occupying lesions such as abscesses, arteriovenous malformations, and infarction, which can have a similar clinical presentation.[8] Other clinical presentations of brain tumors include focal cerebral syndromes such as seizures.[2] Seizures are a presenting symptom in approximately 20% of patients with supratentorial brain tumors and may antedate the clinical diagnosis by months to years in patients with slow-growing tumors. Among all patients with brain tumors, 70% with primary parenchymal tumors and 40% with metastatic brain tumors develop seizures at some time during the clinical course.[9]
Computed tomography (CT) and magnetic resonance imaging (MRI) have complementary roles in the diagnosis of CNS neoplasms.[8,10] The speed of CT is desirable for evaluating clinically unstable patients. CT is superior for detecting calcification, skull lesions, and hyperacute hemorrhage (bleeding less than 24-hours old) and helps direct differential diagnosis as well as immediate management. MRI has superior soft-tissue resolution. MRI can better detect isodense lesions, tumor enhancement, and associated findings such as edema, all phases of hemorrhagic states (except hyperacute), and infarction. High-quality MRI is the diagnostic study of choice in the evaluation of intramedullary and extramedullary spinal cord lesions.[2] In post-therapy imaging, single-photon emission computed tomography (SPECT) and positron emission tomography (PET) may be useful in differentiating tumor recurrence from radiation necrosis.[8]
Biopsy confirmation to corroborate the suspected diagnosis of a primary brain tumor is critical, whether before surgery by needle biopsy or at the time of surgical resection, except in cases where the clinical and radiologic picture clearly point to a benign tumor. Radiologic patterns may be misleading, and a definitive biopsy is needed to rule out other causes of space-occupying lesions, such as metastatic cancer or infection. CT- or MRI-guided stereotactic techniques can be used to place a needle safely and accurately into all but a very few inaccessible locations within the brain.
Specific genetic or chromosomal abnormalities involving deletions of 1p and 19q have been identified for a subset of oligodendroglial tumors, which have a high response rate to chemotherapy.[2,7,11,12,13,14,15] Other CNS tumors are associated with characteristic patterns of altered oncogenes, altered tumor-suppressor genes, and chromosomal abnormalities. Familial tumor syndromes with defined chromosomal abnormalities are associated with gliomas. (Refer to the Classification section of this summary for more information.)
Metastatic Brain Tumors
Brain metastases outnumber primary neoplasms by at least 10 to 1, and they occur in 20% to 40% of cancer patients.[16] Because no national cancer registry documents brain metastases, the exact incidence is unknown, but it has been estimated that 98,000 to 170,000 new cases are diagnosed in the United States each year.[2,8] This number may be increasing because of the capacity of MRI to detect small metastases and because of prolonged survival resulting from improved systemic therapy.[2,16]
The most common primary cancers metastasizing to the brain are lung cancer (50%), breast cancer (15%–20%), unknown primary cancer (10%–15%), melanoma (10%), and colon cancer (5%).[2,16] Eighty percent of brain metastases occur in the cerebral hemispheres, 15% occur in the cerebellum, and 5% occur in the brain stem.[2] Metastases to the brain are multiple in more than 70% of cases, but solitary metastases also occur.[16] Brain involvement can occur with cancers of the nasopharyngeal region by direct extension along the cranial nerves or through the foramina at the base of the skull. Dural metastases may constitute as much as 9% of total CNS metastases.
A lesion in the brain should not be assumed to be a metastasis just because a patient has had a previous cancer; such an assumption could result in overlooking appropriate treatment of a curable tumor. Primary brain tumors rarely spread to other areas of the body, but they can spread to other parts of the brain and to the spinal axis.
The diagnosis of brain metastases in cancer patients is based on the following:
Patients may describe any of the following:
Often, family members or friends may notice the following:
A physical examination may show objective neurological findings or only minor cognitive changes. The presence of multiple lesions and a high predilection of primary tumor metastasis may be sufficient to make the diagnosis of brain metastasis. In the case of a solitary lesion or a questionable relationship to the primary tumor, a brain biopsy (usually a stereotactic biopsy) may be necessary. CT scans with contrast or MRIs with gadolinium are quite sensitive in diagnosing the presence of metastases. PET scanning and spectroscopic evaluation are new strategies to diagnose cerebral metastases and to differentiate the metastases from other intracranial lesions.[17]
Related Summaries
Other PDQ summaries containing information related to adult and childhood brain cancer include the following:
This classification is based on the World Health Organization (WHO) classification of central nervous system (CNS) tumors.[1] The WHO approach incorporates and interrelates morphology, cytogenetics, molecular genetics, and immunologic markers in an attempt to construct a cellular classification that is universally applicable and prognostically valid. Earlier attempts to develop a TNM-based classification were dropped: tumor size (T) is less relevant than tumor histology and location, nodal status (N) does not apply because the brain and spinal cord have no lymphatics, and metastatic spread (M) rarely applies because most patients with CNS neoplasms do not live long enough to develop metastatic disease.[2]
The WHO grading of CNS tumors establishes a malignancy scale based on histologic features of the tumor.[3] The histologic grades are as follows:
WHO grade I includes lesions with low proliferative potential, a frequently discrete nature, and the possibility of cure following surgical resection alone.
WHO grade II includes lesions that are generally infiltrating and low in mitotic activity but recur more frequently than grade I malignant tumors after local therapy. Some tumor types tend to progress to higher grades of malignancy.
WHO grade III includes lesions with histologic evidence of malignancy, including nuclear atypia and increased mitotic activity. These lesions have anaplastic histology and infiltrative capacity. They are usually treated with aggressive adjuvant therapy.
WHO grade IV includes lesions that are mitotically active, necrosis-prone, and generally associated with a rapid preoperative and postoperative progression and fatal outcomes. The lesions are usually treated with aggressive adjuvant therapy.
The following table is from the WHO Classification of Tumours of the Central Nervous System and lists the tumor types and grades.[4] Tumors limited to the peripheral nervous system are not included. Detailed descriptions of histopathology, grading methods, incidence, and what is known about etiology specific to each tumor type can be found in the WHO classification book.[4]
Primary Brain Tumors
Radiation therapy and chemotherapy options vary according to histology and anatomic site of the brain tumor. For high-grade malignant gliomas—glioblastoma, anaplastic astrocytoma, anaplastic oligodendroglioma, and anaplastic oligoastrocytoma—combined modality therapy with resection, radiation, and chemotherapy is standard. Since anaplastic astrocytomas, anaplastic oligodendrogliomas, and anaplastic oligoastrocytomas represent only a small proportion of central nervous system (CNS) gliomas, phase III randomized trials restricted to them are not generally practical. However, since they are aggressive and are often included in studies along with glioblastomas, they are generally managed in a fashion similar to glioblastoma. Therapy involving surgically implanted carmustine-impregnated polymer wafers combined with postoperative external-beam radiation therapy (EBRT) has a role in the treatment of high-grade gliomas regardless of the extent of surgical resection.[1] Specific treatment options for tumor types are listed below under the tumor types and locations. This section covers general treatment principles.
Dexamethasone, mannitol, and furosemide are used to treat the peritumoral edema associated with brain tumors. Use of anticonvulsants is mandatory for patients with seizures.[2]
Finally, active surveillance is appropriate in some circumstances. With the increasing use of sensitive neuroimaging tools, there has been increased detection of asymptomatic low-grade meningiomas. The majority appear to show minimal growth and can often be safely observed, with therapy deferred until the detection of tumor growth or the development of symptoms.[3,4]
For most types of brain tumors in most locations, an attempt at complete or near-complete surgical removal is generally recommended, if possible, within the constraints of preservation of neurologic function and underlying patient health. This recommendation is based on observational evidence that survival is better in patients who undergo tumor resection than in those who have closed biopsy alone.[5,6] However, the benefit of resection has not been tested in randomized trials. Selection bias can enter into observational studies despite attempts to adjust for patient differences that guide the decision to operate. Therefore, the actual difference in outcome between radical surgery and biopsy alone may not be as large as noted in the retrospective studies.[6] An exception to the general recommendation for attempted resection is the case of deep-seated tumors such as pontine gliomas, which are diagnosed on clinical evidence and treated without initial surgery approximately 50% of the time. In most cases, however, diagnosis by biopsy is preferred. Stereotactic biopsy can be used for lesions that are difficult to reach and resect.
Two primary goals of surgery include:[2]
However, total elimination of primary malignant intraparenchymal tumors by surgery alone is rarely achievable. Therefore, intraoperative techniques have been developed to reach a balance between removing as much tumor as is practical and the preservation of functional status. For example, craniotomies with stereotactic resections of primary gliomas can be done in cooperative patients while they are awake, with real-time assessment of neurologic function.[7] Resection proceeds until either the magnetic resonance imaging (MRI) signal abnormality being used to monitor the extent of surgery is completely removed or subtle neurologic dysfunction appears (e.g., slight decrease in rapid alternating motor movement or anomia). Likewise, when the tumor is located in or near language centers in the cortex, intraoperative language mapping can be performed by electrode discharge-induced speech arrest while the patient is asked to count or read.[8]
As is the case with several other specialized operations [9,10] in which postoperative mortality has been associated with the number of procedures performed, postoperative mortality after surgery for primary brain tumors may be associated with hospital and/or surgeon volume.[11] Using the Nationwide Inpatient Sample hospital discharge database for the years 1988 to 2000, which represented 20% of inpatient admissions to nonfederal U.S. hospitals, investigators found that large-volume hospitals had lower in-hospital mortality rates after craniotomies for primary brain tumors (odds ratio [OR] = 0.75 for a ten-fold higher caseload; 95% confidence interval [CI], 0.62–0.90) and after needle biopsies (OR = 0.54; 95% CI, 0.35–0.83). For example, although there was no specific sharp threshold in mortality outcomes between low-volume hospitals and high-volume hospitals, craniotomy-associated in-hospital mortality was 4.5% for hospitals with five or fewer procedures per year and 1.5% for hospitals with at least 42 procedures per year. In-hospital mortality rates decreased over the study years (perhaps because the proportion of elective nonemergent operations increased from 45% to 57%), but the decrease was more rapid in high-volume hospitals than in low-volume hospitals. High-volume surgeons also had lower patient in-hospital mortality rates after craniotomy (OR= 0.60; 95% CI, 0.45–0.79).[11] As with any study of volume-outcome associations, these results may not be causal because they may be affected by residual confounding factors, such as referral patterns, private insurance, and patient selection, despite multivariable adjustment.
Radiation Therapy
High-grade tumors
Radiation therapy has a major role in the treatment of patients with high-grade gliomas. A systematic review and meta-analysis of five randomized trials (plus one trial with allocation by birth date) comparing postoperative radiation therapy (PORT) with no radiation therapy showed a statistically significant survival advantage with radiation (risk ratio = 0.81; 95% CI, 0.74–0.88).[12][Level of evidence: 1iiA] Based on a randomized trial comparing 60 Gy (in 30 fractions over 6 weeks) to 45 Gy (in 25 fractions over 4 weeks) that showed superior survival in the first group (12 months vs. 9 months median survival; hazard ratio [HR] = 0.81; 95% CI, 0.66–0.99), 60 Gy is the accepted standard dose of EBRT for malignant gliomas.[13][Level of evidence: 1iiA]
As with surgical resection, attempts have been made to preserve normal brain function using techniques intended to deliver a full therapeutic dose of radiation to the tumor and a small surrounding margin, while minimizing dose to most of the brain (e.g., 3–dimensional conformal radiation or intensity-modulated radiation therapy [IMRT] and radiosurgery). However, it is not clear that these techniques affect overall survival (OS) compared to standard EBRT.[14] There are no randomized trials directly comparing the effects of these techniques as primary PORT on survival.
A randomized trial tested radiosurgery as a boost added to standard EBRT, but the trial found no improvement in survival, quality of life, or patterns of relapse compared to EBRT without the boost.[14] Based upon a similar rationale, the use of single-fraction stereotactic radiosurgery has disseminated into common practice. High doses of radiation are delivered to the tumor bed with a small margin of nonclinically involved brain. Again, there are no randomized trials that test this concept in comparison to standard radiation.[14]
For the same theoretical reasons, brachytherapy has been used to deliver high doses of radiation locally to the tumor while sparing normal brain tissue. However, this approach is technically demanding and has fallen out of favor with the advent of the above-mentioned techniques.
Low-grade tumors
The role of immediate PORT for low-grade gliomas (i.e., low-grade astrocytoma, oligodendroglioma, mixed oligoastrocytomas) is not as clear as in the case of high-grade tumors. The European Organisation for Research and Treatment of Cancer (EORTC) randomly assigned 311 patients with low-grade gliomas to radiation versus observation in the EORTC-22845 and MRC BR04 trial.[15,16] (On central pathology review, about 25% of the patients on the trial were felt to actually have high-grade tumors.) Most of the control patients received radiation at the time of progression. After a median follow-up of 93 months, median progression-free survival was 5.3 years in the radiation arm versus 3.4 years in the control arm (HR = 0.59; 95% CI, 0.45–0.77).[15,16][Level of evidence: 1iiDiii] However, there was no difference in the OS rate (median survival = 7.4 years vs. 7.2 years; HR = 0.97; 95% CI, 0.71–1.34; P = .87).[15,16][Level of evidence: 1iiA] This was caused by a longer survival after progression in the control arm (3.4 years) than in the radiation arm (1.0 years) (P < .0001). The investigators did not collect reliable quality-of-life measurements, so it is not clear whether the delay in initial relapse in the radiation therapy arm translated into improved function or quality of life.
Repeat radiation therapy (re-irradiation)
Because there are no randomized trials, the role of repeat radiation after disease progression or the development of radiation-induced cancers is also ill defined. The literature is limited to small retrospective case series, which makes interpretation difficult.[17] The decision to use repeat radiation must be made carefully because of the risk of neurocognitive deficits and radiation-induced necrosis. One advantage of radiosurgery is the ability to deliver therapeutic doses to recurrences that may require the reirradiation of previously irradiated brain tissue beyond tolerable dose limits.
Systemic chemotherapy
For many years, the nitrosourea carmustine (BCNU) was the standard chemotherapy added to surgery and radiation for malignant gliomas. This was based upon a randomized trial (RTOG-8302) of 467 patients conducted by the Brain Tumor Study Group that compared four regimens after initial resection:[18]
The radiation therapy plus carmustine arm had the best survival rate.[18][Level of evidence: 1iiA] A modest impact on survival using nitrosourea-containing chemotherapy regimens for malignant gliomas was confirmed in a patient-level meta-analysis of 12 randomized trials (combined HR death = 0.85; 95% CI, 0.78–0.91).[19]
However, the oral agent, temozolomide, has since replaced the nitrosoureas as the standard systemic chemotherapy for malignant gliomas based upon a large multicenter trial (NCT00006353) of glioblastoma patients conducted by the EORTC-National Cancer Institute of Canada (NCIC) that showed a survival advantage.[20,21][Level of evidence: 1iiA] In that study, 573 patients with glioblastoma were randomly assigned to receive standard radiation to the tumor volume with a 2–3 cm margin (60 Gy, 2 Gy per fraction, over 6 weeks) alone or with temozolomide (75 mg/m2 orally per day during radiation therapy for up to 49 days, followed by a 4-week break, and then up to six cycles of five daily doses every 28 days at a dose of 150 mg/m2 increasing to 200 mg/m2 after the first cycle). Patients in the combined therapy group were given prophylactic therapy for Pneumocystis carinii during the period of concomitant radiation therapy and temozolomide. OS was statistically significantly better in the combined radiation therapy/temozolomide group (HR for death = 0.6; 95% CI, 0.5–0.7; survival at 3 years was 16.0% vs. 4.4%).
Localized chemotherapy
Because malignant glioma-related deaths are nearly always the result of an inability to control intracranial disease (rather than the result of distant metastases), the concept of delivering high doses of chemotherapy while avoiding systemic toxicity is attractive. A biodegradable carmustine wafer has been developed for that purpose. The wafers contain 3.85% carmustine, and up to eight wafers are implanted into the tumor bed lining at the time of open resection, with an intended total dose of about 7.7 mg per wafer (61.6 mg maximum per patient) over a period of 2 to 3 weeks. There have been two randomized placebo-controlled trials of this focal drug delivery method, both showing an OS advantage associated with the carmustine wafers. Both trials had an upper age limit of 65 years. The first was a small trial closed after 32 patients with high-grade gliomas had been entered because of a lack of continued availability of the carmustine wafers.[22] Although OS was better in the carmustine-wafer group (median 58.1 vs. 39.9 weeks; P = .012), there was an imbalance in the study arms (only 11 of the16 patients in the carmustine-wafer group vs. 16 of the 16 patients in the placebo-wafer group had Grade IV glioblastoma tumors).
The second study was, therefore, more informative.[23,24] It was a multicenter study of 240 patients with primary malignant gliomas, 207 of whom had glioblastoma. At initial surgery, they received the carmustine versus placebo wafers, followed by radiation therapy (55 Gy–60 Gy). Systemic therapy was not allowed until recurrence, except in the case of anaplastic oligodendrogliomas, of which there were nine patients. Unlike the initial trial, patient characteristics were well balanced between the study arms. Median survival in the two groups was 13.8 months versus 11.6 months; P = .017 (HR = 0.73; 95% CI, 0.56–0.96). A systematic review combining both studies estimated a HR for overall mortality of 0.65; 95% CI, 0.48–0.86; P = .003.[25][Level of evidence: 1iA]
Treatment Options Under Clinical Evaluation
Patients who have brain tumors that are either infrequently curable or unresectable should be considered candidates for clinical trials. Information about ongoing clinical trials is available from the NCI Web site.
Heavy-particle radiation, such as proton-beam therapy, carries the theoretical advantage of delivering high doses of ionizing radiation to the tumor bed while sparing surrounding brain tissue. The data are preliminary for this investigational technique, and it is not widely available.
Novel biologic therapies under clinical evaluation for patients with brain tumors include the following:[26]
Primary Tumors of the Spinal Axis
Surgery and radiation therapy are the primary modalities used to treat tumors of the spinal axis; therapeutic options vary according to the histology of the tumor.[2] The experience with chemotherapy for primary spinal cord tumors is limited; no reports of controlled clinical trials are available for these types of tumors.[2,31] Chemotherapy is indicated for most patients with leptomeningeal involvement (from a primary or metastatic tumor) and positive cerebrospinal fluid cytology.[2] Most patients require treatment with corticosteroids, particularly if they are receiving radiation therapy.
Patients who have spinal axis tumors that are either infrequently curable or unresectable should be considered candidates for clinical trials. Information about ongoing clinical trials is available from the NCI Web site.
Approximately 20% to 40% of cancer patients develop brain metastases, with a subsequent median survival generally less than 6 months. Common primary tumors with brain metastases include the following cancers:
The optimal therapy for patients with brain metastases continues to evolve.[31,32,33] Corticosteroids, anticonvulsants, radiation therapy, radiosurgery, and, possibly, surgical resection have roles in management. Because most cases of brain metastases involve multiple metastases, a mainstay of therapy has historically been whole-brain radiation therapy (WBRT), but stereotactic radiosurgery has come into increasingly common use. The role of radiosurgery continues to be defined. Chemotherapy is usually not the primary therapy for most patients; however, it may have a role in the treatment of patients with brain metastases from chemosensitive tumors and can even be curative when combined with radiation for metastatic testicular germ cell tumors.[32,34] Intrathecal chemotherapy is also used for meningeal spread of metastatic tumors.
Treatment for patients with a single metastasis
About 10% to 15% of patients with cancer will have a single brain metastasis. Radiation therapy is the mainstay of palliation for these patients. The extent of extracranial disease can influence treatment of the brain lesions. In the presence of extensive active systemic disease, surgery provides little benefit for OS. In patients with stable minimal extracranial disease, combined modality treatment may be considered, using surgical resection followed by radiation therapy. However, the published literature does not provide clear guidance. There have been three randomized trials of resection of solitary brain metastases followed by WBRT versus WBRT alone, totaling 195 randomly assigned patients.[35,36,37] The process that necessarily goes into selecting appropriate patients for surgical resection may account for the small numbers in each trial. In the first trial, performed at a single center, all patients were selected and operated upon by one surgeon. The first two trials showed an improvement in survival in the surgery group, but the third showed a trend in favor of the WBRT-only group. The three trials were combined in a trial-level meta-analysis.[25] The combined analysis did not show a statistically significant difference in OS (HR = 0.72; 95% CI, 0.34–1.53; P = .4); nor was there a statistically significant difference in death from neurologic causes (relative risk of death = 0.68; 95% CI, 0.43–1.09; P = .11). None of the trials assessed or reported quality of life. One of the trials reported that combined therapy increased the duration of functionally independent survival.[35][Level of evidence: 1iiD]
The need for WBRT after resection of solitary brain metastases has been tested.[38] Patients in the WBRT group were less likely to have tumor progression in the brain and were significantly less likely to die of neurological causes, but OS was the same, and there was no difference in duration of functional independence.[38] One additional randomized study of observation versus WBRT after either surgery or stereotactic radiosurgery for solitary brain metastases was closed because of slow accrual after 19 patients had been entered, so little can be deduced from the trial.[39] (Refer to the following Treatment for patients with oligometastases (1–3 or 4 brain metastases) section of this summary for evidence of the role of WBRT after focal treatment, whether surgery or stereotactic radiosurgery, in the setting of one to three or four metastases.)
Treatment for patients with oligometastases (1–3 or 4 brain metastases)
A Radiation Therapy Oncology Group (RTOG) study (RTOG-9508) randomly assigned 333 patients with one to three metastases with a maximum diameter of 4 cm to WBRT (37.5 Gy over 3 weeks) with or without a stereotactic boost.[40] Patients with active systemic disease requiring therapy were excluded. The primary endpoint was OS with predefined hypotheses in both the full study population and the 186 patients with a solitary metastasis (and no statistical adjustment of P values for the two separate hypotheses). Mean OS in the combined-therapy and WBRT-alone groups was 5.7 months and 6.5 months, respectively (P = .14). In the subgroup with solitary metastases, OS was better in the combined-therapy group (6.5 months vs. 4.9 months; P =.039 in univariate analysis; P = .053 in a multivariable analysis adjusting for baseline prognostic factors); in patients with multiple metastases, survival was 5.8 months in the combined-therapy group versus 6.7 months in the WBRT-only group (P = .98). (The combined-treatment group had a survival advantage of 2½ months in patients with a single metastasis but not in patients with multiple lesions.) Local control was better in the full population with combined therapy. At the 6-month follow-up, Karnofsky performance status (considered a soft endpoint because of its imprecision and subjectivity) was better in the combined-therapy group, but there was no difference in mental status between the treatment groups. Acute and late toxicities were similar in both treatment arms. Quality of life was not assessed.[40][Levels of evidence: 1iiDii for the full study population and 1iiA for patients with solitary metastases]
The converse question has also been addressed—whether WBRT is necessary after focal treatment (i.e., resection or stereotactic radiosurgery) of oligometastases. Several randomized trials have been performed that were designed with varying primary endpoints.[41,42,43] However, the results can be summarized as follows:
The study that had a primary endpoint of learning and neurocognition, using a standardized test for total recall, was stopped by the data-safety monitoring committee because of worse outcomes in the WBRT group.[42]
Given this body of information, focal therapy plus WBRT or focal therapy alone, with follow-up and initiation of salvage therapy when clinically indicated, appear to be reasonable treatment options. The pros and cons of each approach should be discussed with the patient.[42][Level of evidence: 1iiD]
Treatment for patients with multiple metastases
Patients with multiple brain metastases are treated with WBRT. Surgery is generally restricted to obtaining tissue from metastases with an unknown primary tumor. Stereotactic radiosurgery in combination with WBRT has been assessed and is associated with good local control, but median survival was not affected. Survival was determined by the extent of extracranial disease.[44][Level of evidence: 1iiDii]
Note: Some citations in the text of this section are followed by a level of evidence. The PDQ editorial boards use a formal ranking system to help the reader judge the strength of evidence linked to the reported results of a therapeutic strategy. (Refer to the PDQ summary on Levels of Evidence for more information.)
Brain Stem Gliomas
Standard treatment options:
Brain stem gliomas have relatively poor prognoses that correlate with histology (when biopsies are performed), location, and extent of tumor. The overall median survival time of patients in studies has been 44 to 74 weeks.
Current Clinical Trials
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with adult brain stem glioma. The list of clinical 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.
Pineal Astrocytic Tumors
Depending on the degree of anaplasia, pineal astrocytomas vary in prognoses. Higher grades have worse prognoses.
Pilocytic Astrocytomas
This astrocytic tumor is classified as a World Health Organization (WHO) grade I tumor and is often curable.
Diffuse Astrocytomas
This WHO grade II astrocytic tumor is less often curable than pilocytic astrocytoma.
Anaplastic Astrocytomas
Anaplastic astrocytomas (WHO grade III) have a low cure rate with standard local treatment. Because anaplastic astrocytomas represent less than 10% of all central nervous system gliomas, phase III randomized trials restricted to them are not practical. However, because they are aggressive and often included in studies along with glioblastomas, they are generally managed the same way as glioblastomas, with surgery and radiation, and often with chemotherapy even though it is not known whether the improved survival with chemotherapy in glioblastoma can be extrapolated to anaplastic astrocytomas.
Postoperative radiation alone has been compared to postoperative chemotherapy alone in patients with anaplastic gliomas (i.e., 144 astrocytomas, 91 oligoastrocytomas, and 39 oligodendrogliomas) with crossover to the other modality at the time of tumor progression. One hundred thirty-nine patients were randomly assigned to radiation therapy, and 135 were randomly assigned to chemotherapy with a 32-week course of either procarbazine + lomustine + vincristine (PCV) or single-agent temozolomide (2:1:1 randomization). The order of the modalities did not affect time to treatment failure (TTF) or OS.[2][Levels of evidence: 1iiA and 1iiD] Neither TTF nor OS differed across the treatment arms.
Patients with anaplastic astrocytomas are appropriate candidates for clinical trials designed to improve local control by adding newer forms of treatment to standard treatment. Information about ongoing clinical trials is available from the NCI Web site.
For patients with glioblastoma (WHO grade IV), the cure rate is very low with standard local treatment. These patients are appropriate candidates for clinical trials designed to improve local control by adding newer forms of treatment to standard treatment. Information about ongoing clinical trials is available from the NCI Web site.
Oligodendroglial Tumors
Oligodendrogliomas (WHO grade II) behave like diffuse astrocytomas.
Anaplastic oligodendrogliomas
Anaplastic oligodendrogliomas (WHO grade III) have a low cure rate with standard local treatment, but their prognosis is generally better than that of anaplastic astrocytomas. Since anaplastic oligodendrogliomas are uncommon, phase III randomized trials restricted to them are not practical. They are generally managed with the following:
PORT alone has been compared to postoperative chemotherapy alone in patients with anaplastic gliomas (i.e., 144 astrocytomas, 91 oligoastrocytomas, and 39 oligodendrogliomas) with crossover to the other modality at the time of tumor progression. One hundred thirty-nine patients were randomly assigned to radiation therapy and 135 were randomly assigned to chemotherapy with a 32-week course of either PCV or single-agent temozolomide (2:1:1 randomization). The order of the modalities did not affect TTF or OS.[2][Levels of evidence: 1iiA and 1iiD]. Neither TTF nor OS differed across the treatment arms.
These patients are appropriate candidates for clinical trials designed to improve local control by adding newer forms of treatment. Information about ongoing clinical trials is available from the NCI Web site.
Mixed Gliomas
Mixed glial tumors, which include oligoastrocytoma (WHO grade II) and anaplastic oligoastrocytoma (WHO grade III), have a prognosis similar to that for astrocytic tumors of corresponding grades and can be treated as such.
Ependymal Tumors
Grade I and II ependymal tumors
Ependymomas (WHO grade II) and ependymal tumors (WHO grade I), i.e., subependymoma and myxopapillary ependymomas, are often curable.
Anaplastic ependymomas
Anaplastic ependymomas (WHO grade III) have variable prognoses that depend on the location and extent of disease. Frequently, but not invariably, anaplastic ependymomas have worse prognoses than lower grade ependymal tumors.
Embryonal Cell Tumors: Medulloblastomas
Treatment options under clinical evaluation:
Medulloblastoma occurs primarily in children, but it also occurs with some frequency in adults.[9] Other embryonal tumors are pediatric conditions. (Refer to the PDQ summary on Childhood Central Nervous System Embryonal Tumors Treatment for more information.)
Pineal Parenchymal Tumors
Pineocytoma (WHO grade II), pineoblastoma (WHO grade IV), and pineal parenchymal tumors of intermediate differentiation are diverse tumors that require special consideration. Pineocytomas are slow growing and carry variable prognoses for cure. Pineoblastomas are more rapidly growing and have worse prognoses. Pineal parenchymal tumors of intermediate differentiation have unpredictable growth and clinical behavior.
Meningeal Tumors
Grade I meningiomas
WHO grade I meningiomas are usually curable when resectable. With the increasing use of sensitive neuroimaging tools, there has been greater detection of asymptomatic low-grade meningiomas. The majority appear to show minimal growth and can often be safely observed while therapy is deferred until growth or the development of symptoms.[10,11]
Grade II and III meningiomas and hemangiopericytomas
The prognoses for patients with meningiomas (WHO grade II) (i.e., atypical, clear cell, and chordoid), meningiomas (WHO grade III) (i.e., anaplastic/malignant, rhabdoid, and papillary), and hemangiopericytomas are worse than for patients with low-grade meningiomas because complete resections are less commonly feasible, and the proliferative capacity is greater.
Germ Cell Tumors
The prognosis and treatment of patients with germ cell tumors—which include germinoma, embryonal carcinoma, choriocarcinoma, and teratoma—depend on tumor histology, tumor location, presence and amount of biological markers, and surgical resectability.
Tumors of the Sellar Region: Craniopharyngiomas
Craniopharyngioma (WHO grade I) is often curable.
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with adult brain tumor. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
Re-resection of recurrent brain tumors is used in some patients. However, the majority of patients do not qualify because of a deteriorating condition or technically inoperable tumors. The evidence is limited to noncontrolled studies and case series on patients who are healthy enough and have small enough tumors to technically debulk. The impact of reoperation versus patient selection on survival is not known.
Localized Chemotherapy
Carmustine wafers have been investigated in the setting of recurrent malignant gliomas, but the impact on survival is less clear than at the time of initial diagnosis and resection. In a multicenter randomized, placebo-controlled trial, 222 patients with recurrent malignant primary brain tumors requiring reoperation were randomly assigned to receive implanted carmustine wafers or placebo biodegradable wafers.[1] Approximately half of the patients had received prior systemic chemotherapy. The two treatment groups were well balanced at baseline. Median survival was 31 versus 23 weeks in the two groups. The statistical significance between the two OS curves depended upon the method of analysis. The hazard ratio (HR) for risk of dying in the direct intention-to-treat comparison between the two groups was 0.83 (95% CI, 0.63–1.10; P = .19). The baseline characteristics were similar in the two groups, but the investigators did an additional analysis, adjusting for prognostic factors, because they felt that even small differences in baseline characteristics could have a powerful influence on outcomes. In the adjusted proportional hazards model, the HR for risk of death was 0.67 (95% CI, 0.51–0.90, P = .006). The investigators put their emphasis on this latter analysis and reported this as a positive trial.[1][Level of evidence: 1iA] However, a Cochrane Collaboration systematic review of chemotherapeutic wafers for high-grade glioma focused on the unadjusted analysis and reported the same trial as negative.[2]
Systemic Chemotherapy
Systemic therapy (e.g., temozolomide or the combination of procarbazine, a nitrosourea, and vincristine in patients who have not previously received the drugs) has been used at the time of recurrence of primary malignant brain tumors. However, it has not been tested in controlled studies. Patient-selection factors likely play a strong role in determining outcomes, so the impact of therapy on survival is not clear.
Because there are no randomized trials, the role of repeat radiation after disease progression or the development of radiation-induced cancers is also ill defined. Interpretation is difficult because the literature is limited to small retrospective case series.[3] The decision must be made carefully because of the risk of neurocognitive deficits and radiation necrosis.
Patients who have recurrent brain tumors are rarely curable and should be considered candidates for clinical trials when they have exhausted standard therapy. Information about ongoing clinical trials is available from the NCI Web site.
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with recurrent adult brain tumor. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
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.
Purpose of This Summary
This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the treatment of adult brain tumors. 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 Adult Treatment 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.
The lead reviewer for Adult Brain Tumors Treatment is:
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 Adult Treatment Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
Permission to Use This Summary
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® Adult Brain Tumors Treatment. Bethesda, MD: National Cancer Institute. Date last modified <MM/DD/YYYY>. Available at: http://cancer.gov/cancertopics/pdq/treatment/adultbrain/HealthProfessional. Accessed <MM/DD/YYYY>.
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Liberty News
Chelanga defends national cross country champion title
|Sam Chelanga competes in the NCAA Division I national cross country championship in Terre Haute, Ind. on Monday.
Liberty redshirt senior Sam Chelanga claimed his second consecutive NCAA national title in his final collegiate cross country race on Monday.
Chelanga is now a three-time NCAA Division I national champion, also including his 10K crown at the 2010 NCAA Division I Outdoor Track & Field Championships.
Also earning All-America honors for the Flames on Monday was redshirt senior Evans Kigen. He clocked a 30:21.4 to finish 31st place overall out of 246 finishers.
- Read the full story at www.libertyflames.com.


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Fourth Time's the Charm...Nipple Piercing Oddessy
This is the story of my four year, four-times pierced journey to finally having female nipple piercings.
I decided to get my nipples pierced not long after my first piercing (nostril). I was 31 at the time. My breasts and nipples are both very large, but not that sensitive. I read that piercing them would make them much more sensitive and decided to go for it. I read that healing could take a long time, and since I wasn't sexually active at the time, it seemed like a good time to go for it.
The first time I got them pierced, I went to a place I found online. I was very nervous. I didn't know anyone else who was into body modification, and my source of information was the internet. At the time, it seemed like like a really extreme piercing (oh, how things change!). I chose the place I went to because when I looked at their site online, they had pictures of female genital piercings. I figured that if they did genital piercings, they shouldn't look at me too funny when I asked for my nipples done.
The piercer spent a long time talking to me about aftercare (about an hour). I later discovered that most of what he recommended was correct. He also used good, sterile techniques. He then finally piercing the nipples using 14 guage 1/2" CBRs. I paid and left (unfortunately, this was before I knew to tip). He even scheduled a follow-up appointment. So I figured he knew what he was doing.
I discovered from friends I'd met online that the rings he used were too small. I ordered and inserted larger rings. I discovered from painful experience that I don't like healing my nipples using rings. They inevitable slide around, drag lymph into my piercings, and generally hurt like hell despite wearing a bra. They also had a tendency to stick straight out and didn't want to lie flat (probably because they were too small). After about a month, I took them out.
Of course, then I decided I wanted to try again! This time I decided to get pierced with barbells. The piercer recommended 12 gauge, so that's what I went with. By now I knew a lot more about piercing, so I went to a piercer recommended by my tattoo artist who is also a member of APP (he was focused more on tattooing at the time, which is why he didn't do their piercing himself). The piercing and healing process both went well. The barbells were definitely much more comfortable and I really wish I had left them in, as they were nearly completely healed when I took them out almost 6 months later. But I felt strange walking around as a Christian women with nipple rings, so I removed them. (Yes, I am still a Christian.)
Third piercing: by now I had met my husband, who is also a Christian and has pierced nipples himself. I was really excited to get them repierced. I went to a third piercer (now my regular one) who is also a member of APP, and got pierced using 12guage barbells again. This time was a disaster (not the piercer's fault). First, my left breast swelled like mad, so I had to switch to longer bars. I should have gone in and had him do it, since it would have been free, but I did it myself. I ended up changing jewelry too often. I have always thought that rings were very sexy, so I put some in even though as I mentioned above I find them uncomfortable. Also, I let my husband play with and lick my boobs after a couple months.
About 3 months or so into healing, my left boob suddenly got very hot and painful. I took out the piercing (stupid idea!!!). The redness started streaking across my breast and was probably about 2 inches in size, so my husband made me go to the doctor. Luckily, the doctor did not make a big deal out the fact that I'd had my nipple pierced, but it turned out I had cellulitis, and I almost had to have surgery for an abscess. I had to get a breast ultrasound and take both IV and oral antibiotics and very high doses. If I'd had better insurance I probably would have wound up in the hospital.
But every time I looked at my husband's nipple piercings, I missed mine. I think nipple piercings are very sexy. And as I mentioned, my breasts are not that sensitive. Without my bars in, my nipples were flat. So after thinking a LONG time, I got them repierced. This time I am being fanatical about aftercare. I've only changed jewelry once; when the long initial bar snagged on something, I changed to a shorter bar. I've continued my aftercare, using H2Ocean spray and saline soaked Qtips to gently wipe lymph off the bars and touching/sliding/rotating them as little as possible. I wear a tank top or bra to bed every night and my husband has not touched them. It's been three months and they are healing beautifully with no problems at all. I intend to keep up my aftercare until a full 6 months.
So female nipples are quite an oddessy to heal but I think it is worth it and I plan to keep these in!
submitted by: goldshadow
on: 27 June 2011


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Though he may not have walked away with any hardware at this year's CMA Awards , singer-songwriter Lee Brice is rounding out the year far from empty-handed.
"I'm really probably at one of the best times in my life," he recently told reporters during an informal gathering at Loser's Bar & Grill, a local hotspot near downtown Nashville. "I'm happy in my personal life and my family and in my career. I really am at one of the high points of my life that I can ever remember."
Besides garnering his first CMA nomination for new artist of the year, Brice also reached platinum-selling and chart-topping success as an artist with "A Woman Like You." Having written smash hits for artists like Garth Brooks ("More Than a Memory") and the Eli Young Band ("Crazy Girl" ), he is thrilled to now be reaping recognition as not only a songwriter but also a bona fide artist.
"My fans have been my career," he said. "We've worked hard to build a foundation. Now, anything extra has just been icing on the cake."
His current single, "Hard to Love," the title track from his sophomore album, has already sold over 500,000 copies and recently secured the top spot of Billboard's country songs chart, making this his second No. 1 as an artist.
"We've been working so hard for so long, and I can't be more thankful to songwriters that wrote such a great song and especially for being my friends as a person and as a writer," he explained. "They know me well enough to write a song that I could connect with so well, and I'm just so lucky to be where I'm at."
Written by fellow song-craftsmen Benjamin Glover, Billy Montana and John Ozier, Brice explained how the lyrics seemed as though they were written with him in mind.
"It felt like I was in the room writing it," he said of the first time he heard the charismatic tune.
"If I'm going to record a song I didn't write, I literally have to connect with it as if I wrote it," he went on. "So then when I'm singing it, I'm sellin' it and livin' it as much as I would have if it was one I wrote."
What's more, Brice said his entire life has prepared him for this moment. Writing songs since he was just 10, he always wanted to be an artist who sang his own songs.
"This is really what I've been working for, so it feels awesome," he explained.
Another shot in the arm came recently while waiting for his bus inside Tin Roof, a popular bar and restaurant near Nashville's Music Row. The television series Nashville was piping through the bar's speakers when he heard a familiar tune.
"I heard this song playing, and I was like, 'I know that song! Oh, I wrote that song!'" he laughed. "I didn't know I had a song on there. Man, that's my song. Awesome!"
Hoping to continue his career momentum, Brice assured reporters he's already secured a spot alongside a major touring act in 2013. Though he wouldn't reveal details, he confirmed it was a "pretty major tour."
Not one to slow down and always looking ahead, Brice said he's preparing to record his third album in January.
"Sometimes I may just reach too far," he said of his ambitious personality. "By 2014, I want to be able to go and do arenas. That's my goal. Now, if I get to that, I don't know. That's kind of how I've always lived my life — really shooting high."


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Grouse Moors -Environmental devastation
The Estate owners and shooting associations are quick to make huge claims of how the work they do benefits the moorland and the environment. What they don't mention is that they are paid huge subsidies by the Government (that's our money) to maintain bio-diverse habitats and ecosystems, rich in flora and fauna, but this is not what they are doing.
What they are doing is creating a monoculture environment based on heather for the benefit of one species - grouse. The so-called traditional management of the land consists of burning and vegetation control. Traditionally, moorland was burnt on a 30-year rotation to create a mosaic of different habitats. Due to the intensity of the grouse being raised to be shot for so called 'sport', this rotation is now under 10 years and dropping.
Critically, these moors supply up to 70% of the UK's drinking water, filtered through peat bogs. The management of the land for grouse and heather includes burning more land, more often, including protected peat bogs. Peat was a traditional fuel used by crofters for generations; it burns slowly, even underground and destroys the peat bog habitat and everything that depends upon it.
The increased burning leaves huge 'patchwork areas' where rainwater, rather than soaking into the traditional moorland and peat bogs, can only 'run-off' the surface. This is the primary reason why we have seen such a dramatic increase in flooding in our rural towns and villages as the river and flood protection systems cannot cope with the deluge running off the hills.
But even that isn't it - every one of us is paying higher water bills because the water companies now have to filter the water from the moors, simply because shooting estates burn peat bogs. Burning causes Dissolved Organic Carbon (DOC) and discolouration of the water.
The Save Me Trust is appalled at the level of taxpayers money that supports the shooting estates and their poor conservation of our rich and diverse natural environment. When you understand the real costs of subsidies, water treatment and the increased risk of flooding, the monetary costs are substantial, but the cost to the flora and fauna of our environment is irreparable.
Please donate to support our campaign here:


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We are all too familiar with the murder of helpless babies within the womb. Now it is being extended. New born babies are being murdered in the UK--all "legally" of course, under the loving embrace of the National Health Service. One UK doctor has become a whistleblower.
This report is republished from The Blaze:
UK Doctor's Horrifying Admission Reveals How Sick & Disabled Babies Are Put on 'Death Pathways', Deprived of Food & Fluid for 10 Days
Sick children and even disabled newborn babies, are reportedly being discharged from NHS hospitals in England only to die slowly at home or in hospices in an unfathomable manner. The innocent children are being put on controversial "death pathways," once only thought to have involved elderly and terminally ill adult patients.
The Liverpool Care Pathway (LCP), an organization that facilitates end-of-life treatment, is behind the inhumane program. The Daily Mail has learned the process of "withdrawing food and fluid by tube is being used on young patients as well as severely disabled newborn babies." In other words, patients — young and old — are slowly starved and dehydrated to death.
One doctor, acting as a whistle blower, admitted to starving and dehydrating ten babies to death in the neonatal unit of one hospital in a leading medical journal. The doctor describes it as a 10-day process, during which the baby becomes "smaller and shrunken."
Roughly 130,000 elderly and terminally ill patients reportedly die on the Liverpool Care Pathway, or "death pathways." LCP is now being independently investigated at the orders of ministers in England.
The Daily Mail has more details on this tragic story:
The investigation, which will include child patients, will look at whether cash payments to hospitals to hit death pathway targets have influenced doctors' decisions. Medical critics of the LCP insist it is impossible to say when a patient will die and as a result the LCP death becomes a self-fulfilling prophecy. They say it is a form of euthanasia, used to clear hospital beds and save the NHS money.Here's some of what the doctor wrote in the medical journal [emphasis added]:
The use of end of life care methods on disabled newborn babies was revealed in the doctors' bible, the British Medical Journal. The previously mentioned doctor wrote of the pain of watching the slow, forced deaths of newborn babies. One baby's parents decided to put their infant on the "pathway" because of a "lengthy list of unexpected congenital anomalies," according to the doctor.
The voice on the other end of the phone describes a newborn baby and a lengthy list of unexpected congenital anomalies. I have a growing sense of dread as I listen. The parents want 'nothing done' because they feel that these anomalies are not consistent with a basic human experience. I know that once decisions are made, life support will be withdrawn.After reading the article in the British Medical Journal, Dr. Laura de Rooy, a consultant neonatologist at St. George's Hospital NHS Trust in London, wrote on the BMJ website: "It is a huge supposition to think they do not feel hunger or thirst."
Assuming this baby survives, we will be unable to give feed, and the parents will not want us to use artificial means to do so. Regrettably, my predictions are correct. I realise as I go to meet the parents that this will be the tenth child for whom I have cared after a decision has been made to forgo medically provided feeding.
Like other parents in this predicament, they are now plagued with a terrible type of wishful thinking that they could never have imagined. They wish for their child to die quickly once the feeding and fluids are stopped. They wish for pneumonia. They wish for no suffering. They wish for no visible changes to their precious baby.
Their wishes, however, are not consistent with my experience. Survival is often much longer than most physicians think; reflecting on my previous patients, the median time from withdrawal of hydration to death was ten days.
"The LCP was devised by the Marie Curie Palliative Care Institute in Liverpool for care of dying adult patients more than a decade ago. It has since been developed, with [pediatric] staff at Alder Hey Hospital, to cover children. Parents have to agree to their child going on the death pathway, often being told by doctors it is in the child's 'best interests' because their survival is 'futile'," The Daily Mail reports.
Obviously, not everyone agrees. Bernadette Lloyd, a hospice pediatric nurse, wrote to the Cabinet Office and the Department of Health and blasted the use of death pathways for young children. "The parents feel coerced, at a very traumatic time, into agreeing that this is correct for their child whom they are told by doctors has only has a few days to live," she wrote. "It is very difficult to predict death. I have seen a reasonable number of children recover after being taken off the pathway."
She went on: "I have also seen children die in terrible thirst because fluids are withdrawn from them until they die…I witnessed a 14 year-old boy with cancer die with his tongue stuck to the roof of his mouth when doctors refused to give him liquids by tube. His death was agonising for him, and for us nurses to watch. This is euthanasia by the backdoor."
For now the inquiry into the death pathways is ongoing. A Department of Health spokesman said that "End of life care for children must meet the highest professional and clinical standards, and the specific needs of children at the end of their life." But as Teresa Lynch, a spokeswoman for the Medical Ethics Alliance, points out: "There are big questions to be answered about how our sick children are dying."
To read more of the anonymous doctor's testimony in the British Medical Journal, click here.


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Current Theme Song (aka what's playing on my ipod right now): Turn of a Friendly Card, Part 2 by Alan Parsons Project
Now here it is, front and center: my first contest ever. And it's big. And I mean BIG. And it is so easy. I tried to think of every possible way you could win. The prize? Simply any book you want in the entire world. No joke. One book, under $50, no questions asked. It doesn't even have to be in print. Yes, I have my diabolical ways. It's all a part of being Writer-Girl (though if it is out of print, an ISBN number helps immensely). If I were to win – definitely Diana Wynn Jones' Howl's Moving Castle, first edition, hardcover (I'm a sucker for hardcovers). Or The Arrival by Shaun Tan. But I can't win, lucky you. So, comment away, there are about a million ways you can get "points" – entries with your name on it. It's all in your court. Let's get this party started! Contest closes Saturday May 2nd, on the digital turn of midnight.
3 points: become a follower (and you can see yourself over on that side bar. So cute)
1 point: Commenting, even saying "yo." (note: "yo" comment only works once. Of course, this would be a perfect time to tell which book you want me to send you)
1 point: Commenting with email address and/blog address: (2 potential points).
1 point: Giving favorite blogs/websites. You have to say why.
3 points: Mentioning this on your blog: (an extra point if you tell everyone to add it too. 4 potential points).
2 points: Comment and say what superhero you are (because you are whether you see it or not).
Uh… (trying to think of more ways you can rack up points)…
1 point: Adding me in Google Reader or similar RSS feeder
2 points: Telling me what else I can give you points for.
10 points for whoever can get me mentioned on Nathan Bransford's blog ;) (If you can do that, I'll buy you a book outright). ^_^
To those twelve subscribers who followed my previous version of this blog: 2 extra points to you. Thanks for sticking around from the beginning. I know who most of you are, but you have to comment to get the point! And those lurkers I don't know had better come forward. I'm looking at you, wherever you are.
Big Contest, I mean BIG.
Current Theme Song (aka what's playing on my ipod right now): Turn of a Friendly Card, Part 2 by Alan Parsons Project
38 comments:
- PJ Hoover said...
I'm just psyched I'm the FIRST follower!!!! Whoo hooo!
- April 14, 2009 at 7:35 AM
- Vivian said...
Love the new blog--the artwork is fantastic! Nice job!
- April 14, 2009 at 8:13 AM
- Alysa Stewart said...
Ok let's see... do I have to do separate comments for more points? oh, why not. It is always fun to have a high comment count! Yo!
- April 14, 2009 at 9:27 AM
- Alysa Stewart said...
Oh, and I LOVE the setup here! It is super cute, and more importantly it is READABLE! On another note, I think your name is very interesting and that you could've stuck with your old URL just fine.
- April 14, 2009 at 9:28 AM
- Alysa Stewart said...
Umm, you have my email address, and if you don't it is posted on my blog. My blog, of course is http://everead.blogspot.com
Speaking of... I'd love to have you write up a guest review sometime! So anytime you've read a good book that is so good you just want to spread the love, let me know! (this goes for other people reading this post. nothing like a good guest review about a good book!)
- April 14, 2009 at 9:30 AM
- Alysa Stewart said...
I am Ruby Diamond. That is my superhero name. My superpowers are many and varied.
- April 14, 2009 at 9:32 AM
- Alysa Stewart said...
You could give me points for sending you an awesome personalized email...
- April 14, 2009 at 9:33 AM
- Alysa Stewart said...
How many points do I have now?
- April 14, 2009 at 9:33 AM
- Alysa Stewart said...
You could give me points for adding you to my blogroll on Everead... (That is what I'm going to do instead of adding you to my feed or following. I am switching to blog rolls for my own sanity and the health and well-being of my family.)
- April 14, 2009 at 9:35 AM
- Alysa Stewart said...
I don't know which book I would want you to send me yet. There are SO many good ones that I want. But one favorite of mine that is out of print (oh! I just love it!) is Pickle Things by Marc Tolon Brown.
- April 14, 2009 at 9:37 AM
- Alysa Stewart said...
So, will you be using your old blog at all? Ever again?
- April 14, 2009 at 9:38 AM
- Heather Zundel said...
Well yo right back! ^_^
This is fantastic! And Alysa, dang girl, you're pulling out all the stops, aren't you? Let's see. . . you've got. . . 11 points so far. I gave you 2 points for email idea (not a bad one!) and an extra bonus point for sincerely talking to me in the comments. You are so sweet. And yes! I would love to do a guest post sometime. Just tell me when. You are still missing the biggest point-getters though. You get 3 points each for mentioning this on your blog AND for being a follower. Dang, I'm impressed.
And thank you Vivien and PJ! I did try to find a template that really looked good. And you both were old subscibers. So you've got your two extra points (and I love your enthusiasm PJ!)
(Oh, and Alysa, I don't know if I'll use the old one again. I haven't gotten that far in my planning. But I'm certainly not deleting it, that's for sure!) And thank you about my name. You're gonna make me blush.
- April 14, 2009 at 10:11 AM
- Kelsey said...
Heather! I'm liking the new blog! LOVE the layout! So cute! But I'll be sad to see A Daily Muse go. I really liked the title of that blog too.
I'm proud to now become a follower (though I would've even if you didn't have this awesome contest!)
A superhero? Me? Hmm...if I had to say what type of superhero to be it would be that I am the super enchilada cooker girl. I make the BEST chicken enchiladas. Haha.
- April 14, 2009 at 2:29 PM
- Katie said...
I just became a follower!
- April 14, 2009 at 2:43 PM
- Katie said...
Email: email@example.com
Blog address: http://katiesbookshelf11.blogspot.com/
- April 14, 2009 at 2:44 PM
- Katie said...
One of my favorite websites is thestorysiren.com. It had lots of great book reviews, author interviews, and contests.
- April 14, 2009 at 2:45 PM
- Katie said...
You can give me points for complimenting your layout. I love the plants and patterns!
- April 14, 2009 at 2:47 PM
- Katie said...
My "yo" comment: Hi! I just found your blog and I'm liking it so far. I'm interested to see what you have in store for future posts. =]
- April 14, 2009 at 2:48 PM
- Unknown said...
Yo! I LOVE the new layout!! So awesome!!
- April 14, 2009 at 6:39 PM
- Heather Zundel said...
Kelsey - I'm surprised so many (even if it is just two) have expressed sadness at my old blog's passing. Maybe I can extend it's life somehow. . . no promises yet. I loved that title too.
Hello Katie! You are a new face, right? I just checked out your blog and it's AWESOME. I'm going to be putting it into my reader as soon as I can. It looks like I have a lot of reading to catch up on. And I'll think about a point for the compliment ;)
Beth! Good to see you made it over. That makes me really happy. Don't forget to spread the word!
- April 15, 2009 at 7:36 PM
- LoraliSophia said...
- April 15, 2009 at 7:56 PM
- Anonymous said...
Sheesh. I am trying to cut DOWN on my Google reader feeds, woman! But I am a sucker for a pretty blog, and I love your template.
(Does that count as a yo? And I started following, but mostly because I like seeing my picture on other people's blogs.)
- April 20, 2009 at 1:16 PM
- KR said...
I'm following.
- April 20, 2009 at 3:19 PM
- KR said...
Yo, I'd get childrens books for my clasroom. I teach kindergarten. It's hard to find giveaways for good kiddy lit!!
- April 20, 2009 at 3:20 PM
- KR said...
Email addy
- April 20, 2009 at 3:20 PM
- KR said...
I'd SuperMom. I have Mommy Magic. I ALWAYS know who really did it!!!
- April 20, 2009 at 3:22 PM
- KR said...
Extra points///it's my 32nd year of teaching..that deserves something...right?????
- April 20, 2009 at 3:22 PM
- PurpleClover said...
You can find me at http://purpleclover-purpleclover.blogspot.com and my email is firstname.lastname@example.com.
I love agentquery.com because it lists all the agencies that work in your genre with just a simple click of the button...even has links to their website! I also love querytracker.net because you can keep track of your lovely queries and responses! They also have a blog that you can get to from that website and they do fun contests as well.
I'm a superhero because I'm the best butt wiper in the whole nursing school I attend. And if The Wiper wasn't here who else would get the job done?? (Certainly not most of my classmates). I'm also a mom of two kids, working a part time job, writing a novel, and going to school full time. Superhero? (any other day I would tell you how i fail miserably but for the points...for the points). I really need to get war and peace and don't want to spend the dough...lol.
You could give me points for mentioning you on Nathan's blog. I'd be happy to post it in the comments. :) lol.
Come on over to my blog! Take your shoes off and stay a while.
- April 20, 2009 at 3:59 PM
- PurpleClover said...
(I didn't use it yet so I figured it didn't hurt)
- April 20, 2009 at 4:00 PM
- Heather Zundel said...
Aerin, sorry to add to your reader. I know it's hard, but so well worth it. And hey, who wouldn't like seeing their picture on other people's blogs? :)
MJ, you've come to the right place for a good kiddy-lit contest! And kindergarten! I would love to see what books you read to your kids. We may have to swap picture book favorites. (And you totally get an extra point for teaching 32 years. That is awesome!)
PurpleClover, I LOVE your superhero identity!!! I wasn't expecting to laugh and I almost choked on my pop tart. And you will totally get a point for mentioning me in the comments of Nathan's blog. And I'm heading to your blog right now. (And good job with the 'yo' I had no idea that would take off so well. Or my template. I'm tickled pink so many people like it) ^_^
LoraliaSophia - yo right back at ya. :)
- April 21, 2009 at 6:00 PM
- Liyana said...
I'm a follower, also on Google subscriber! My yo comment would be: Welcome to the YA blogosphere. Well, technically I've only discovered your site now. :D And the book: Jessica's Guide To Dating The Dark Side by Beth Fantaskey.
My favourite blog: http://thestorysiren.com
http://twitter.com (Do I need a reason? :P)
http://nathanbransford.blogspot.com/ (All the tips on publishing...)
I'm a superhero who can heal people with just a thought. On the other hand, I can hurt them with a thought too, but since I'm a superHERO, I try to do good things. LOL.
Oh, you could so totally give me points for linking you to these two blogs where people can get to know of your blog:
My email: email@example.com
My blog: http://liveandbreathesmexily.blogspot.com
Have fun!
- April 27, 2009 at 1:47 PM
- Heather Zundel said...
Wow, look at you being all compact and all. That's awesome! And you are totally getting points for those blog links. And I love your superHERO-ness. That is an awesome skill, and one I wish I had.
- April 30, 2009 at 8:05 AM
- Reyna Meinhardt said...
3 points: I became a follower to your GREAT blog! I love the layout!
1 point: Hmm, this is my comment saying "yo" so I will say, "YO!" I would have said which book I want, however, it might take me a while to decide :)
1 point: firstname.lastname@example.com
1 point: www.booksforteensreviews.blogspot.com
1 point: Storysiren.com. I love Kristi's blog because it is so well organized, she has a great way to write reviews, and she does this in a friendly way! Plus, I also love Vania's blog, http://reveriemedia.blogspot.com/ because of its awesome layout, the way Vania posts her posts, and how she puts up a handmade cover by her every Saturday that looks like it was made professionally! Plus, Vania's super nice!
2: Hmm, you could give extra points for saying what book is your favorite, ONE of mine is "The Season" by Sarah MacLean.
10: I'll try but don't give me the points just yet (and don't cross your fingers either, lol!)
Thanks for the great contest!!
- April 30, 2009 at 10:18 AM
- Shooting Stars Mag said...
Let's see here, I'm comenting, so that counts yes?
email: Lauren51990 AT aol DOT com
Blog: www.shootingstarsmag.blogspot.com
I'm now a follower.
A favorite blog or website? Well, I love panic at the disco dot com or whatever it is, b/c the band is cool but also b/c i'm a part of the online book club on their message boards and those girls are rad!
I am a super awesome superhero. True that. I can go anywhere I want by thinking about it and I fight crime, but I don't HURT the bad guy. Just help.
Wellll....you could give me points for complimenting you. "You are looking quite lovely today, did you do something to your hair?" ;-)
- April 30, 2009 at 11:01 AM
- Luvdaylilies said...
My goodness,I find you on the very last day! I like the blog & the giveaway is beyond wonderful=)
Luvdaylilies at bellsouth dot net
- May 2, 2009 at 6:15 PM
- Luvdaylilies said...
Just to let you know, I became a follower=)
Luvdaylilies at bellsouth dot net
- May 2, 2009 at 6:17 PM
- Anonymous said...
Okay, +4 from previous post
+2: aerinblogs AT aol DOT com
+3 added in my sidebar
+1: RSS Reader
+2: My Superhero power is speed reading (actually, that's true) and my quest is to make every book feel loved. And my mascot is a purple seahorse.
+1: favorite blog & websites are Hello Ello (elloecho.blogspot.com) because she's funny and uber-smart; and Lean On The Wind (leanonthewind.blogspot.com) because its my sister's
I think Beth should get extra points for pointing me here because I've been having fun with your posts this week (I'm not a huge commenter).
I humbly think I should receive extra points for making you a SuperHero Badge (even though it needs tweaking; too pixelated; but I just threw it together):
SO, my lovely, that makes a total of 13 points plus whatever you deem appropriate for the badge.
- May 2, 2009 at 7:59 PM
- Anonymous said...
or an azure alien. As my mascot. Hmm. I have to think about that.
- May 2, 2009 at 8:00 PM