text:
Hypocalcemia

Hypocalcemia is a medical condition characterized by low calcium levels in the blood serum. The normal range of blood calcium is typically between 2.1–2.6 mmol/L (8.8–10.7 mg/dL, 4.3–5.2 mEq/L), while levels less than 2.1 mmol/L are defined as hypocalcemic. Mildly low levels that develop slowly often have no symptoms. Otherwise symptoms may include numbness, muscle spasms, seizures, confusion, or in extreme cases cardiac arrest.

The most common cause for hypocalcemia is iatrogenic hypoparathyroidism. Other causes include other forms of hypoparathyroidism, vitamin D deficiency, kidney failure, pancreatitis, calcium channel blocker overdose, rhabdomyolysis, tumor lysis syndrome, and medications such as bisphosphonates or denosumab. Diagnosis should generally be confirmed by determining the corrected calcium or ionized calcium level. Specific changes may also be seen on an electrocardiogram (ECG).

Initial treatment for severe disease is with intravenous calcium chloride and possibly magnesium sulfate. Other treatments may include vitamin D, magnesium, and calcium supplements. If due to hypoparathyroidism, hydrochlorothiazide, phosphate binders, and a low salt diet may also be recommended. About 18% of people who are being treated in hospital have hypocalcemia.

Signs and symptoms
The neuromuscular symptoms of hypocalcemia are caused by a positive bathmotropic effect (i.e. increased responsiveness) due to the decreased interaction of calcium with sodium channels. Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers, reduced calcium lowers the threshold for depolarization. The symptoms can be recalled by the mnemonic "CATs go numb" - convulsions, arrhythmias, tetany, and numbness in the hands and feet and around the mouth. • Petechiae which appear as on-off spots, then later become confluent, and appear as purpura (larger bruised areas, usually in dependent regions of the body).

• Oral, perioral and acral paresthesias, tingling or 'pins and needles' sensation in and around the mouth and lips, and in the extremities of the hands and feet. This is often the earliest symptom of hypocalcaemia.

• Carpopedal and generalized tetany (unrelieved and strong contractions of the hands, and in the large muscles of the rest of the body) are seen.

• Latent tetany

• * Trousseau sign of latent tetany (eliciting carpal spasm by inflating the blood pressure cuff and maintaining the cuff pressure above systolic)

• * Chvostek's sign (tapping of the inferior portion of the cheekbone will produce facial spasms)

• Tendon reflexes are hyperactive

• Life-threatening complications

• * Cardiac arrhythmias

• Effects on cardiac output

• * Negative chronotropic effect, or a decrease in heart rate.

• * Negative inotropic effect, or a decrease in contractility

• *

• ECG changes include the following:

• * Intermittent QT prolongation, or intermittent prolongation of the QTc (corrected QT interval) on the ECG (electrocardiogram) is noted. The implications of intermittent QTc prolongation predisposes to life-threatening cardiac electrical instability (and this is therefore a more critical condition than constant QTc prolongation). This type of electrical instability puts the person at high risk of torsades de pointes, a specific type of ventricular tachycardia which appears on an EKG (or ECG) as something which looks a bit like a sine wave with a regularly increasing and decreasing amplitude. (Torsades de pointes can cause death, unless the person can be medically or electrically cardioverted and returned to a normal cardiac rhythm.)

Causes
Hypoparathyroidism is a common cause of hypocalcemia. Calcium is tightly regulated by the parathyroid hormone (PTH). In response to low calcium levels, PTH levels rise, and conversely if there are high calcium levels then PTH secretion declines. However, in the setting of absent, decreased, or ineffective PTH hormone, the body loses this regulatory function, and hypocalcemia ensues. Hypoparathyroidism is commonly due to surgical destruction of the parathyroid glands. Hypoparathyroidism may also be due to autoimmune problem. Some causes of hypocalcaemia are as follows:

• Hyperphosphatemia

• Vitamin D deficiency

• Chronic liver disease

• Edetate disodium

• Magnesium deficiency

• Prolonged use of medications/laxatives (magnesium)

• Osteomalacia

• Chronic kidney failure

• Ineffective active vitamin D

• Hypoparathyroidism/genetic

• After surgery hypoparathyroidism

• Hungry bone syndrome

• Tumour lysis syndrome

• Acute kidney injury

• Rhabdomyolysis (initial stage)

• As a complication of pancreatitis

• Alkalosis

• Massive red blood cell transfusion due to excess citrate in the blood

• As blood plasma hydrogen ion concentration decreases, caused by respiratory or metabolic alkalosis, the concentration of freely ionized calcium, the biologically active component of blood calcium, decreases. Because a portion of both hydrogen ions and calcium are bound to serum albumin, when blood becomes alkalotic, the bound hydrogen ions dissociate from albumin, freeing up the albumin to bind with more calcium and thereby decreasing the freely ionized portion of total serum calcium. For every 0.1 increase in pH, ionized calcium decreases by about 0.05 mmol/L. This hypocalcaemia related to alkalosis is partially responsible for the cerebral vasoconstriction that causes the lightheadedness, fainting, and paraesthesia often seen with hyperventilation.

• Neonatal hypocalcemia

• Gain of function mutations of the calcium-sensing receptor

• Foscarnet use

• Loop diuretic use

• Crohn disease

• High level of lactic acid in the blood

• Pseudohypoparathyroidism

• Trauma

Mechanism
Physiologically, blood calcium is tightly regulated within a narrow range for proper cellular processes. Calcium in the blood exists in three primary states: bound to proteins (mainly albumin), bound to anions such as phosphate and citrate, and as free (unbound) ionized calcium. Only the unbound ionized calcium is physiologically active. Normal blood calcium level is between 8.5 and 10.5 mg/dL (2.12 to 2.62 mmol/L) and that of unbound calcium is 4.65 to 5.25 mg/dL (1.16 to 1.31 mmol/L).

Diagnosis

Because a significant portion of calcium is bound to albumin, any alteration in the level of albumin will affect the measured level of calcium. A corrected calcium level based on the albumin level is: Corrected calcium (mg/dL) = measured total Ca (mg/dL) + 0.8 * (4.0 - serum albumin [g/dL]). Since calcium is also bound to small anions, it may be more useful to correct total calcium for both albumin and the anion gap.

Management
Management of this condition includes:
 * Intravenous calcium gluconate 10% can be administered, or if the hypocalcaemia is severe, calcium chloride is given instead. This is only appropriate if the hypocalcemia is acute and has occurred over a relatively short time frame. But if the hypocalcemia has been severe and chronic, then this regimen can be fatal, because there is a degree of acclimatization that occurs. The neuromuscular excitability, cardiac electrical instability, and associated symptoms are then not cured or relieved by prompt administration of corrective doses of calcium, but rather exacerbated. Such rapid administration of calcium would result in effective over correction – symptoms of hypercalcemia would follow.
 * However, in either circumstance, maintenance doses of both calcium and vitamin-D (often as 1,25-(OH)2-D3, i.e. calcitriol) are often necessary to prevent further decline.

title: Hypocalcemia


text:
User talk:Bcorr/Archive 200402

Archived talk from February 2004

• Moroccan Cuisine
Wouldn't it be easier to make the real edit in the first place? -- BCorr ¤ Брайен 02:32, 25 Feb 2004 (UTC)

 * What I wrote was accurate. What I replaced was somewhere on the scale from culturally niave to racist.  I was not insulting.  I did not say "filthy, lecherous Westerners".  You reverted.  You could have done the edit you suggest I do.  You have corrected me but you have not corrected Wikipedia.  If you are concerned about Wikipedia then you should remove the pre-exisiting inaccurate insult.  Otherwise please explain the motivation for your action.

 * I don't monitor others' Talk pages. Reply to mine, please.

 * Paul Beardsell 02:41, 25 Feb 2004 (UTC)

 * My point is simple. If there's a problem, correct it. Adding facetious text in in attempt to get someone else to fix the problem you found is not generally productive. Thanks, BCorr ¤ Брайен 02:58, 25 Feb 2004 (UTC)

 * To make my point more plain: Imagine if on the American Cuisine page there was the equally misleading comment Kentucky Fried Chicken is usually eaten at brothels.  Paul Beardsell 03:00, 25 Feb 2004 (UTC)

 * and that was replaced by KFC is sometimes fed to North African tourists at so-called restaurants.

 * Then I would change it without adding something about overfed Americans eating ersatz Southern cuisine at a multinational fast-food chain... -- BCorr ¤ Брайен 03:03, 25 Feb 2004 (UTC)

 * In reply: You also had the opportunity but did not take it.  The reversion  was unnecessary policing.  With the same effort you could have made the constructive change you want me to make.  You have blindly crossed the street to correct a jay walker.  Paul Beardsell 03:06, 25 Feb 2004 (UTC)

 * Whatever -- BCorr ¤ Брайен 03:17, 25 Feb 2004 (UTC)

 * To make your point about how I could act more constructively you reverted a Wikipedia article to an inaccurate version. That's "whatever".  Paul Beardsell 03:28, 25 Feb 2004 (UTC)

 * For the record, my change was not of the above character, but was unemotive and factual. What BCorr is objecting to (I think) is the phrasing of the comment I made about my change.  The actual edit is itself difficult to object to as it is both unemotionally phrased and accurate.  It is not "facetious", as alleged.  View the moroccan cuisine version log and diffs.  Paul Beardsell 03:44, 25 Feb 2004 (UTC)

''I have copied the above text to the Moroccan Cuisine talk page. Paul Beardsell 03:54, 25 Feb 2004 (UTC)''

• Paul Vogel rants again
"A supremacist [snip] at all costs."

STOP MIS-REDIRECTING THIS NPOV ARTICLE TO A MARXIST-PC POV. THANKS! User:24.45.99.191

 * We will continue to revert your edits to remove your POV about what you claim are differences between white supremacists and white separatists. -- BCorr ¤ Брайен 18:11, 25 Feb 2004 (UTC)

It is NOT my claim, it is the actual NPOV distinction between them, and whether your own POV actually thinks there is one or NOT!

---

"A supremacist [snip] to avoid at all costs."

(text added by Paul Vogel, abridged by BCorr)

• The user I blocked
Well, I just thought about it and I was wrong to use an extended block for a single incident of vandalism. I'll keep an eye out though. Pakaran. 21:07, 25 Feb 2004 (UTC)

 * By the time you posted this, they'd already reinserted the samuel jepson stuff. But I think you did the right thing. I think I'll go block them for a day unless someone beats me to it. BCorr ¤ Брайен 21:11, 25 Feb 2004 (UTC)

• Paul Vogel reprise
Thanks! Glad to see a sysop hard at work! Perl 02:05, 26 Feb 2004 (UTC)

 * We aim to please! I'll just redelete it and remove it from Vfd. -- BCorr ¤ Брайен 02:07, 26 Feb 2004 (UTC)

 * "Hard at work" only preventing any truely NPOV articles from actually ever seeing the light of day! What a cabal of Marxist-pc POV bigots and censors!

 * Maybe I'm just a Wikisupremacist...or is that Wikiseparatist? -- BCorr ¤ Брайен 02:42, 26 Feb 2004 (UTC)

 * No, neither, just a wiki F-head! That's only being objective and accurate and with a typically here, "Wiki NPOV!" LOL! :D (added by Paul Vogel)

 * That there are two words might suggest there is a difference in the meaning between them. What does the DICTIONARY say.  Ah!  [That I can see a difference does not make me a supporter of either concept.]  Paul Beardsell 02:49, 26 Feb 2004 (UTC)

 * [and it is that I comment on this page that makes me point that out.] Paul Beardsell 03:17, 26 Feb 2004 (UTC)

 * He can format it but he can't reply to it. Paul Beardsell 04:02, 26 Feb 2004 (UTC)

 * Here is my reply, oh snippy and demanding one: White separatist-- BCorr ¤ Брайен 04:26, 26 Feb 2004 (UTC)

 * Well, I'm happier now. Nice article.  (pat).  Snippy is a bit rich from you.  (slap).  Paul Beardsell 04:37, 26 Feb 2004 (UTC)

It seems to me that much of the heat in this discussion could have been defused by an admission early on that a difference between separatism and supremacism is acknowledged but that a NPOV form of words was being sought. Now that difference is acknowledged. That is really all the non-supremacist separatists (whether you believe their position is tenable or not) wanted. It seems to me that some of the unseemly language, however regrettable, was provoked. Paul Beardsell 04:49, 26 Feb 2004 (UTC)

• Deleting new pages in other languages
Hi, I have been recently made admin and am just trying out the deletion of new pages by vandals. I just want to clarify a doubt seeing that you are one of the admins online now. Is it good form to delete something written in, apparently, another language? Thanks KRS 16:20, 26 Feb 2004 (UTC)

 * Hi KRS -- I think that's OK, but I'm relatively new -- I just moved it to the German Wikipedia to be nice, but I'm not sure what it said as I speak very little German. In fact, I just made a user page over there in case it comes up again (if you haven't heard there was a story about Wikipedia on a major German TV network yesterday, so there's a LOT of new traffic -- both on the German and on the English Wikipedia) and I discoved that part of the title of the article is the German for "Edit this page." Oh well -- I imagine someone there will fix or delete it.

 * Anyway, you might want to post a message at Village pump. It would be a good time to revisit the policy -- assuming we have one.

 * Cheers, BCorr ¤ Брайен 16:33, 26 Feb 2004 (UTC)

• Transliteration/transcription
''Hello Cantus -- I've been ignoring your edits to hockey and tennis players, but we do have standards, and altering the Soviet Union article is a bit too much. Thanks, BCorr ¤ Брайен 19:20, 26 Feb 2004 (UTC)''
 * Hello, what exactly was a bit too much? I'm confused by your message. You claim to be 'ignoring' some of my changes. I do not know what this means (reverting?). And what standards are you talking about? Thanks.

 * When I said "standards", a more precise term sould have been "conventions." Because we are creating an encyclopedia, it is important that there is internal consistency -- especially for thiks like country articles. See WikiProject_Countries for more info, and Russia, Dagestan, etc. for examples of the current conventions. If you think that they are wrong, please discuss that at Talk:WikiProject_Countries and the community will weigh in and will come to a collective decision. -- BCorr ¤ Брайен 19:48, 26 Feb 2004 (UTC)

• In vikipaedia veritas
Carpe diem! Aut vincere aut mori! Deus vult! Ceteris paribus. ;-) Ex animo, Evercat 23:59, 26 Feb 2004 (UTC) List of Latin phrases is my friend... Evercat

• Corrections sur certaines pages
Bonjour, je vois que tu parles très bien le français, alors je m'adresse à toi dans ma langue. Hier, j'ai fait plusieurs corrections sur la fiche de l'Ecole polytechnique, et tu les as aussitôt remodifiées. Il s'agissait de french/French et du E avec un accent aigu. Autant je reconnais que j'ai sans doute fait une erreur au niveau des majuscules des adjectifs anglais (je croyais qu'on ne mettait une majuscule que lorsqu'une nationalité était utilisée comme un nom: an American, et pas lorsqu'elle était utilisée comme adjectif),

mais pour ce qui concerne le E avec un accent aigu, je ne suis pas du tout d'accord avec toi: la langue française interdit les accents sur les majuscules; en plus je trouve ce caractère laid. Je te laisse donc le soin de vérifier mes dires, et de faire les éventuelles corrections encore nécessaires. Dans tous les cas, merci pour tes contributions à Wikipedia...

 * Merci beaucoup de votre réponse. Je comprends votre point, et oui, je sais que cela en français l'accent aigu n'est pas employé sur les majuscules.  Cependant, en anglais nous les employons, parce que nous ne sommes pas en tant que familier avec lequel les mots exigent des accents.  Je ne suis pas sûr de l'utilisation conventionnelle sur le Wikipédia français, mais sur le Wikipédia anglais nous préférons toujours employer l'utilisation anglaise standard.  Par exemple, nous employons Quebec -- pas Québec parce que c'est l'utilisation anglaise.  De la même manière, nous continuons à employer des accents aigus sur les majuscules, en dépit de l'interdiction de l'Académie Française.

 * Voir aussi Naming conventions (use English), et aucun exemples -- Fencing et École Polytechnique de Montréal

 * Sincèrement, BCorr ¤ Брайен 14:12, 27 Feb 2004 (UTC)

• Corzine
thanks for the help with Jon Corzine... you were one step ahead of me with the pic and stuff. Its pretty much done as of now, however you can should look it over and change whatever

ZackDude 02:09, 28 Feb 2004 (UTC)

 * Happy to help. Peace, BCorr ¤ Брайен 02:13, 28 Feb 2004 (UTC)

• Images
Your placement code was fine, but it's more complicated than necessary now that the extended image syntax is in place. :) --Minesweeper 02:28, Feb 28, 2004 (UTC)

===• Сою́з Сове́тских Социалисти́ческих Респу́блик === Meet me at the Village pump. Mikkalai

 * I've posted a proposal there and created a place for discussion at Wikipedia_talk:Naming_conventions_(places). See you there?

-- BCorr ¤ Брайен 03:11, 28 Feb 2004 (UTC)

• Thanks all around
That jerk vandal was beginning to tire me out.:) -- Decumanus 03:31, 28 Feb 2004 (UTC)

 * No problem -- thank you! -- BCorr ¤ Брайен 03:35, 28 Feb 2004 (UTC)

An IP is blocked if there's any entry in the block table - I'll unblock and reblock now... Pakaran. 03:32, 28 Feb 2004 (UTC)

 * Thanks for the help -- I'm eager, but still pretty new...

• Lukashenko
Re Lukashenka and Lukashenko: I don't have a strong opinion about this one way or the other. Lukashenko is more common in English, but that is because it is the Russian form. Belarusians would obviously prefer we used the Belarusian spelling, and I don't see any problem with that. (We now say Belarus rather than Byelorussia, so it would seem logical to be consistent). I am in favour of retaining traditional English forms for historical figures (Phillip II rather than Felipe II, for example), but for current figures the tendency in the media is more and more to use an "authentic" spelling rather than an anclicised one. Provided there are redirects from one to the other I doubt it matters much. Adam 05:45, 28 Feb 2004 (UTC)

 * Thanks Adam -- I appreciate the feedback. BCorr ¤ Брайен 05:51, Feb 28, 2004 (UTC)

I'd love to help - but I know nothing of Russian :(. Maybe ask on the pump?  Pakaran. 06:57, 28 Feb 2004 (UTC)

 * Actually User:Mikkalai already got this going down at the pump -- and if you haven't dropped by already, you may discover that you could be of help after all. Thanks again, BCorr ¤ Брайен 15:19, Feb 28, 2004 (UTC)

Thanks for your note - i support you 100% PMA 06:58, Feb 28, 2004 (UTC)

 * Thank you! BCorr ¤ Брайен 15:19, Feb 28, 2004 (UTC)

• In Canto non est veritas
Cantus has edited my contribution to the discussion and changed the words - now i am pissed off - can you do something to stop him? PMA 15:40, Feb 28, 2004 (UTC)

 * I see Bcorr has reverted your changes, PMA at Wikipedia_talk:Naming conventions (places). But Bcorr why did you remove what Cantus had written below PMA's contribution. It seemed pretty reasonable and surely just removing a reasonable comment may serve to anatagonize? Pete/Pcb21 (talk) 16:23, 28 Feb 2004 (UTC)

 * PMA -- I left some more advice at User talk:Cantus. And Pete -- it was a mistake -- I keep forgetting that my sysop rollback function reverts to the last user, not the last edit. I'm going to go fix it now....Thanks for the heads up! -- BCorr ? Брайен 16:30, Feb 28, 2004 (UTC)

 * He didn't "correct" what i wrote he _changed_ it - look at the Mikhail Gorbachev article from before i edited it. he edited my comment in the discussion - changing his "original" written Gorbachev pronounciation (which i had copied to the discusion to show how he even got prtonounciations wrong even though he wants them in the articles) to something else. _That_ is what upsets me BC :( PMA 16:45, Feb 28, 2004 (UTC)

 * Ok -- I didn't realize the full extent of what he had done -- that's far more than a simple breach of Wikiquette. I'll give some though to the next step, as I doubt he's going to change his ways -- he may be well on his way to being banned. Thanks again, BCorr ? Брайен 19:53, Feb 28, 2004 (UTC)

• Tks for response
Thanks BCorr for your quick response on my talk page. Bender said he was quoting from a book, and that's what bothered me. However, my main worry is that he is using decimalised imperial measurement. It's either decimal and/or imperial in my experience. I can't see why anyone would need to write 2.75 feet for something that is 2ft 9 in long. Cheers Moriori 01:49, Feb 29, 2004 (UTC)

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: User talk:Bcorr/Archive 200402


text:
Hypercalcaemia

Hypercalcemia, also spelled hypercalcaemia, is a high calcium (Ca2+) level in the blood serum. The normal range is 2.1–2.6 mmol/L (8.8–10.7 mg/dL, 4.3–5.2 mEq/L), with levels greater than 2.6 mmol/L defined as hypercalcemia. Those with a mild increase that has developed slowly typically have no symptoms. In those with greater levels or rapid onset, symptoms may include abdominal pain, bone pain, confusion, depression, weakness, kidney stones or an abnormal heart rhythm including cardiac arrest.

Most outpatient cases are due to primary hyperparathyroidism and inpatient cases due to cancer. Other causes of hypercalcemia include sarcoidosis, tuberculosis, Paget disease, multiple endocrine neoplasia (MEN), vitamin D toxicity, familial hypocalciuric hypercalcaemia and certain medications such as lithium and hydrochlorothiazide. Diagnosis should generally include either a corrected calcium or ionized calcium level and be confirmed after a week. Specific changes, such as a shortened QT interval and prolonged PR interval, may be seen on an electrocardiogram (ECG).

Treatment may include intravenous fluids, furosemide, calcitonin, intravenous bisphosphonate, in addition to treating the underlying cause. The evidence for furosemide use, however, is poor. In those with very high levels, hospitalization may be required. Haemodialysis may be used in those who do not respond to other treatments. In those with vitamin D toxicity, steroids may be useful. Hypercalcemia is relatively common. Primary hyperparathyroidism occurs in 1–7 per 1,000 people, and hypercalcaemia occurs in about 2.7% of those with cancer.

Signs and symptoms
The neuromuscular symptoms of hypercalcaemia are caused by a negative bathmotropic effect due to the increased interaction of calcium with sodium channels. Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers, increased calcium raises the threshold for depolarization. This results in decreased deep tendon reflexes (hyporeflexia), and skeletal muscle weakness.

Other symptoms include cardiac arrhythmias (especially in those taking digoxin), fatigue, nausea, vomiting (emesis), loss of appetite, abdominal pain, & paralytic ileus. If kidney impairment occurs as a result, manifestations can include increased urination, urination at night, and increased thirst. Psychiatric manifestation can include emotional instability, confusion, delirium, psychosis, and stupor. Calcium deposits known as limbus sign may be visible in the eyes.

Symptoms are more common at high calcium blood values (12.0 mg/dL or 3 mmol/L). Severe hypercalcaemia (above 15–16 mg/dL or 3.75–4 mmol/L) is considered a medical emergency: at these levels, coma and cardiac arrest can result. The high levels of calcium ions decrease the neuron membrane permeability to sodium ions, thus decreasing excitability, which leads to hypotonicity of smooth and striated muscle. This explains the fatigue, muscle weakness, low tone and sluggish reflexes in muscle groups. The sluggish nerves also explain drowsiness, confusion, hallucinations, stupor or coma. In the gut this causes constipation. Hypocalcaemia causes the opposite by the same mechanism.

Hypercalcaemic crisis
A hypercalcaemic crisis is an emergency situation with a severe hypercalcaemia, generally above approximately 14 mg/dL (or 3.5 mmol/L).

The main symptoms of a hypercalcaemic crisis are oliguria or anuria, as well as somnolence or coma. After recognition, primary hyperparathyroidism should be proved or excluded.

In extreme cases of primary hyperparathyroidism, removal of the parathyroid gland after surgical neck exploration is the only way to avoid death. The diagnostic program should be performed within hours, in parallel with measures to lower serum calcium. Treatment of choice for acutely lowering calcium is extensive hydration and calcitonin, as well as bisphosphonates (which have effect on calcium levels after one or two days).

Causes
Primary hyperparathyroidism and malignancy account for about 90% of cases of hypercalcaemia.

Causes of hypercalcemia can be divided into those that are PTH dependent or PTH independent.

Parathyroid function

 * Primary hyperparathyroidism
 * Solitary parathyroid adenoma
 * Primary parathyroid hyperplasia
 * Parathyroid carcinoma
 * Multiple endocrine neoplasia (MEN1 & MEN2A)
 * Familial isolated hyperparathyroidism
 * Lithium use
 * Familial hypocalciuric hypercalcemia/familial benign hypercalcemia

Cancer
Hypercalcemia of malignancy (cancer) is due to a variety of mechanisms. The two most common are humoral hypercalcemia of malignancy and local osteolytic hypercalcemia due to bony metastasis. Humoral hypercalcemia of malignancy involves the tumor releasing a hormone which increases calcium mobilization (most commonly parathyroid hormone-related protein (PTHrP)) into the circulation. PTHrP acts similarly to parathyroid hormone in that it binds to the parathyroid hormone 1 receptors on the kidneys and bones and causes an increased tubular reabsorption of calcium and activation of osteoclast activity, respectively. Osteoclasts are a type of bone cell which cause bone resorption, releasing calcium into the bloodstream. PTHrP also acts by activating rank ligand and inhibiting osteoprotegerin which activates nuclear factor kappa B, which causes further activation of osteoclast activity. The combination of PTHrP driven osteoclast activation and calcium reabsorption by the kidneys causes hypercalcemia associated with malignancy (humoral type).

Another mechanism in which cancer causes hypercalcemia is via local osteolysis due to metastasis to bone. Tumor bone metastasis releases local cytokines including IL-6, IL-8, IL-11, interleukin-1 beta, TNF alpha and macrophage inflammatory protein. These cytokines activate osteoclasts and inhibit osteoblasts (the cell type responsible for laying down new bone) via the rank ligand pathway leading to bone resorption and calcium release into the bloodstream. The massive release of calcium from bone metastasis and osteoclast activation usually overwhelms the kidney's ability to secrete calcium, thus leading to hypercalcemia.

Hypercalcemia of malignancy may also occur due to tumor production of Vitamin D or parathyroid hormone. These causes are rare and constitute about 1% of all causes of hypercalcemia of malignancy.

Hypercalcemia of malignancy usually portends a poor prognosis, and the medial survival is 25–52 days of its development. It has an incidence of 30% in those with cancer, and the prevalence is estimated to be about 2-3% in the United States.

Common cancer types that are associated with hypercalcemia of malignancy include:

 * Solid tumor with metastasis via local osteolytic hypercalcemia: which can be due to any tumor that metastasizes to the bone. But common causes include breast cancer, lung cancer, kidney cancer, and myeloma or lymphoma of the bone
 * Solid tumor with humoral mediation of hypercalcemia: lung cancer (especially squamous cell tumors, a type of non-small cell lung cancer), squamous cell cancers of the head and neck, kidney cancer or other urothelial cancers, and breast cancer.
 * Hematologic cancers: including multiple myeloma, lymphoma, leukemia
 * Ovarian small cell carcinoma of the hypercalcemic type

Vitamin-D disorders

 * Hypervitaminosis D (vitamin D intoxication)
 * Elevated 1,25(OH)2D (see calcitriol under Vitamin D) levels (e.g. sarcoidosis and other granulomatous diseases such as tuberculosis, berylliosis, histoplasmosis, Crohn's disease, and granulomatosis with polyangiitis)
 * Idiopathic hypercalcaemia of infancy
 * Rebound hypercalcaemia after rhabdomyolysis

High bone-turnover

 * Hyperthyroidism
 * Multiple myeloma
 * Prolonged immobilization
 * Paget's disease
 * Thiazide use
 * Vitamin A intoxication

Kidney failure

 * Tertiary hyperparathyroidism
 * Aluminium intoxication
 * Milk-alkali syndrome

Other

 * Acromegaly
 * Adrenal insufficiency
 * Zollinger–Ellison syndrome
 * Williams Syndrome
 * Excessive calcium consumption

Diagnosis
Diagnosis should generally include either a calculation of corrected calcium or direct measurement of ionized calcium level and be confirmed after a week. This is because either high or low serum albumin levels does not show the true levels of ionised calcium. There is, however, controversy around the usefulness of corrected calcium as it may be no better than total calcium.

Once calcium is confirmed to be elevated, a detailed history taken from the subject, including review of medications, any vitamin supplementations, herbal preparations, and previous calcium values. Chronic elevation of calcium with absent or mild symptoms often points to primary hyperparathyroidism or Familial hypocalciuric hypercalcemia. For those who has underlying malignancy, the cancers may be sufficiently severe to show up in history and examination to point towards the diagnosis with little laboratory investigations.

If detailed history and examination does not narrow down the differential diagnoses, further laboratory investigations are performed. Intact PTH (iPTH, biologically active parathyroid hormone molecules) is measured with immunoradiometric or immunochemoluminescent assay. Elevated (or high-normal) iPTH with high urine calcium/creatinine ratio (more than 0.03) is suggestive of primary hyperparathyroidism, usually accompanied by low serum phosphate. High iPTH with low urine calcium/creatinine ratio is suggestive of familial hypocalciuric hypercalcemia. Low iPTH should be followed up with Parathyroid hormone-related protein (PTHrP) measurements (though not available in all labs). Elevated PTHrP is suggestive of malignancy. Normal PTHrP is suggestive of multiple myeloma, vitamin A excess, milk-alkali syndrome, thyrotoxicosis, and immobilisation. Elevated Calcitriol is suggestive of lymphoma, sarcoidosis, granulomatous disorders, and excessive calcitriol intake. Elevated calcifediol is suggestive of vitamin D or excessive calcifediol intake.

The normal range is 2.1–2.6 mmol/L (8.8–10.7 mg/dL, 4.3–5.2 mEq/L), with levels greater than 2.6 mmol/L defined as hypercalcaemia. Moderate hypercalcaemia is a level of 2.88–3.5 mmol/L (11.5–14 mg/dL) while severe hypercalcaemia is > 3.5 mmol/L (>14 mg/dL).

ECG
Abnormal heart rhythms can also result, and ECG findings of a short QT interval suggest hypercalcaemia. Significant hypercalcaemia can cause ECG changes mimicking an acute myocardial infarction. Hypercalcaemia has also been known to cause an ECG finding mimicking hypothermia, known as an Osborn wave.

Treatments
The goal of therapy is to treat the hypercalcaemia first and subsequently effort is directed to treat the underlying cause. In those with a calcium level above 13 mg/dL, calcium level that is rising rapidly or those with altered mental status, urgent treatment is required.

Fluids and diuretics
Initial therapy:
 * IV fluids is the initial therapy. Hypercalcemia usually causes symptoms that lead to chronic dehydration, such as nausea, vomiting, anorexia, and nephrogenic diabetes insipidus (inability of the kidney to concentrate the urine). IV fluid rehydration allows the kidneys to excrete more calcium, and usually lowers the calcium level by 1–2 mg/dL.
 * increased salt intake also can increase body fluid volume as well as increasing urine sodium excretion, which further increases urinary calcium excretion.
 * after rehydration, a loop diuretic such as furosemide can be given to permit continued large volume intravenous salt and water replacement while minimizing the risk of blood volume overload and pulmonary oedema. In addition, loop diuretics tend to depress calcium reabsorption by the kidney thereby helping to lower blood calcium levels
 * caution must be taken to prevent potassium or magnesium depletion

Bisphosphonates and calcitonin
Additional therapy:
 * bisphosphonates are pyrophosphate analogues with high affinity for bone, especially areas of high bone-turnover.
 * they are taken up by osteoclasts and inhibit osteoclastic bone resorption, therefore inhibiting calcium release from osteoclasts
 * current available drugs include: (1st generation) etidronate, (2nd generation) tiludronate, IV pamidronate, alendronate (3rd generation) zoledronate and risedronate
 * Bisphosphonates are used as a first line therapy for those with hypercalcemia of malignancy. They are used as both an acute therapy and are usually continued long term to prevent hypercalcemia.
 * Bisphosphonates are not recommended in those with chronic kidney disease or those who are severely dehydrated as they may worsen or cause kidney disease.
 * Bisphosphonates caused normalization of calcium levels in 60-90% of patients who were treated for hypercalcemia of malignancy.
 * Denosumab is a bone anti-resorptive agent that can be used to treat hypercalcemia in patients with a contraindication to bisphosphonates such as severe kidney failure or allergy.
 * Denosumab is a monoclonal antibody that inhibits osteoclasts. It acts by binding RANK ligand preventing it from activating osteoclasts via NFKB.
 * Denosumab caused normalization of calcium levels in 70% in those with hypercalcemia of malignancy.
 * Calcitonin blocks bone resorption by inhibiting osteoclasts and also increases urinary calcium excretion by the kidneys.
 * Usually used in life-threatening hypercalcaemia along with rehydration, diuresis, and bisphosphonates
 * Due to its limited duration of action (it works for 48–96 hours, then efficacy decreases as the calcitonin receptors are downregulated) its use is limited to acute hypercalcemia as a bridge therapy until more long-term treatments can be initiated.

Other therapies

 * rarely used, or used in special circumstances:
 * plicamycin inhibits bone resorption (rarely used)
 * gallium nitrate inhibits bone resorption and changes structure of bone crystals (rarely used)
 * glucocorticoids increase urinary calcium excretion and decrease intestinal calcium absorption
 * no effect on calcium level in normal or primary hyperparathyroidism
 * effective in hypercalcemia due to malignancy with elevated vitamin D levels (many types of malignancies raise the vitamin D level).
 * also effective in hypervitaminosis D and sarcoidosis
 * dialysis usually used in severe hypercalcaemia complicated by kidney failure. Supplemental phosphate should be monitored and added if necessary
 * phosphate therapy can correct the hypophosphataemia in the face of hypercalcaemia and lower serum calcium, but this can further increase the risk for kidney stones and nephrocalcinosis

Other animals
Research has led to a better understanding of hypercalcemia in non-human animals. Often the causes of hypercalcemia have a correlation to the environment in which the organisms live. Hypercalcemia in house pets is typically due to disease, but other cases can be due to accidental ingestion of plants or chemicals in the home. Outdoor animals commonly develop hypercalcemia through vitamin D toxicity from wild plants within their environments.

Household pets
Household pets such as dogs and cats are found to develop hypercalcemia. It is less common in cats, and many feline cases are idiopathic. In dogs, lymphosarcoma, Addison's disease, primary hyperparathyroidism, and chronic kidney failure are the main causes of hypercalcemia, but there are also environmental causes usually unique to indoor pets. Ingestion of small amounts of calcipotriene found in psoriasis cream can be fatal to a pet. Calcipotriene causes a rapid rise in calcium ion levels. Calcium ion levels can remain high for weeks if untreated and lead to an array of medical issues. There are also cases of hypercalcemia reported due to dogs ingesting rodenticides containing a chemical similar to calcipotriene found in psoriasis cream. Additionally, ingestion of household plants is a cause of hypercalcemia. Plants such as Cestrum diurnum, and Solanum malacoxylon contain ergocalciferol or cholecalciferol which cause the onset of hypercalcemia. Consuming small amounts of these plants can be fatal to pets. Observable symptoms may develop such as polydipsia, polyuria, extreme fatigue, or constipation.

Outdoor animals
In certain outdoor environments, animals such as horses, pigs, cattle, and sheep experience hypercalcemia commonly. In southern Brazil and Mattewara India, approximately 17 per cent of sheep are affected, with 60 per cent of these cases being fatal. Many cases are also documented in Argentina, Papua New Guinea, Jamaica, Hawaii, and Bavaria. These cases of hypercalcemeia are usually caused by ingesting Trisetum flavescens before it has dried out. Once Trisetum flavescens is dried out, the toxicity of it is diminished. Other plants causing hypercalcemia are Cestrum diurnum, Nierembergia veitchii, Solanum esuriale, Solanum torvum, and Solanum malacoxylon. These plants contain calcitriol or similar substances that cause rises in calcium ion levels. Hypercalcemia is most common in grazing lands at altitudes above 1500 meters where growth of plants like Trisetum flavescens is favorable. Even if small amounts are ingested over long periods of time, the prolonged high levels of calcium ions have large negative effects on the animals. The issues these animals experience are muscle weakness, and calcification of blood vessels, heart valves, liver, kidneys, and other soft tissues, which eventually can lead to death.

title: Hypercalcaemia


text:
Barré Studio

Barré Studio was among the first film studios dedicated to animation and founded by Raoul Barré and William Nolan in 1914. The studio pioneered some early animation processes, including mechanical perforation of cels and animating special effects on glass.

The studio began with advertising films (among the first animated films used to sell something), then got a series with Edison called the Animated Grouch Chaser. The series was mostly live-action with a few animated inserts. The studio also put out the Phables and The Boob Weekly cartoons. Animators included Frank Moser, Gregory La Cava, George Stallings, Tom Norton and Pat Sullivan, all of whom got their starts here. Rube Goldberg was the writer for The Boob Weekly.

In 1916, William Randolph Hearst founded International Film Service, and hired all of Barré's animators to work for him, including Bill Nolan. Soon afterward, Barré was contacted by Charles Bowers, who had been animating Mutt and Jeff for a year. The series was doing so well that it had outgrown Bowers' studio. A partnership was formed: Bowers' animators and series worked on in Barré's studio. The result was the Bud Fisher Film Corporation, named for the originator Bud Fisher of the Mutt and Jeff comic strip. It was known in the industry as the Barré-Bowers Studio.

Fisher took all public credit for the cartoons, while Barré supervised the animators and Bowers handled the books. He "handled" the books so well, in fact, that he ruined the company: Barré quit in 1918 to avoid getting charged as an accomplice; Bowers was fired in 1919 and 1921. This left Fisher in charge. Barré-Bowers went bankrupt in 1923.

Besides Barré and Bowers, directors at their studio included Manny Gould and Dick Friel. Animators included C. T. Anderson, Clarence Rigby, George Stallings, Ted Sears, Mannie Davis, Burt Gillett, Dick Huemer, Tom Palmer, Ben Sharpsteen, Bill Tytla, Albert Hurter, Carl Lederer, F. M. Follett, Isadore Klein, Milt Gross, Walter Lantz and George Ruffle.

Filmography
Series
 * Animated Grouch Chasers (1915)
 * Phables (1915-1916)
 * The Boob Weekly (1916)
 * Mutt and Jeff (1916-1926)

One-Shots
 * Cartoons On A Yacht (1915)

title: Barré Studio


text:
Robert Ripley

LeRoy Robert Ripley (February 22, 1890 – May 27, 1949) was an American cartoonist, entrepreneur, and amateur anthropologist, who is known for creating the Ripley's Believe It or Not! newspaper panel series, television show, and radio show, which feature odd facts from around the world.

Subjects covered in Ripley's cartoons and text ranged from sports feats to little-known facts about unusual and exotic sites. He also included items submitted by readers, who supplied photographs of a wide variety of small-town American trivia ranging from unusually shaped vegetables to oddly marked domestic animals, all documented by photographs and then depicted by his drawings.

Biography
LeRoy Robert Ripley was born on February 22, 1890, in Santa Rosa, California, although his exact birthdate is disputed. He dropped out of high school after his father's death to help his family, and at age 16, he began working as a sports cartoonist for various newspapers. In 1913, he moved to New York City. While drawing cartoons for The New York Globe newspaper, he created his first "Believe It or Not!" cartoon, published in the December 19, 1918, issue. With a positive response from readers, the cartoon began appearing weekly.

In 1919, Ripley married fourteen-year-old film actress Beatrice Roberts, a child 15 years his junior. He made his first trip around the world in 1922, publishing his travel journal in the newspapers. He became fascinated with unusual and exotic foreign locales and cultures. Because he took the veracity of his claims quite seriously, in 1923, he hired a researcher and polyglot named Norbert Pearlroth as a full-time assistant. In 1926, Ripley's cartoons moved from the New York Globe to the New York Post.

Throughout the 1920s, Ripley continued to broaden the scope of his work and his popularity increased greatly. He published a guide to the game of American handball in 1925. In 1926, he became the New York State handball champion and also wrote a book on boxing. With a proven track record as a versatile writer and artist, he attracted the attention of publishing mogul William Randolph Hearst, who managed the King Features Syndicate. In 1929, Hearst was responsible for Believe It or Not! making its syndicated debut in 360 newspapers and 17 languages worldwide. With the success of this series assured, Ripley capitalized on his fame by getting the first book collection of his newspaper panel series published.

On November 3, 1929, he drew a panel in his syndicated cartoon saying "Believe It or Not, America has no national anthem." Despite the widespread belief that "The Star-Spangled Banner", with its lyrics by Francis Scott Key set to the music of the English drinking song "To Anacreon in Heaven", was the United States national anthem, Congress had never officially made it so. In 1931, John Philip Sousa published his opinion in favor of giving the song official status, stating, "it is the spirit of the music that inspires" as much as it is Key's "soul-stirring" words. By a law signed on March 3, 1931, by President Herbert Hoover, "The Star-Spangled Banner" was adopted as the national anthem of the United States.

Ripley prospered during the Great Depression, netting $500,000 a year by the end of the 1930s. He employed a large staff of researchers, artists, translators, and secretaries to handle a deluge of suggestions for new oddities to report – and he traveled the world in search of curiosities and expanded his media to include radio and Hollywood. He started building museums in major cities. Funding for Ripley's highly publicized global travels were provided by the Hearst organization. Always in search of the bizarre, he recorded live radio shows underwater and from the sky, the Carlsbad Caverns, the bottom of the Grand Canyon, snake pits, and other exotic locales. The next year, he hosted the first of a series of two dozen Believe It or Not! theatrical short films for Warner Bros. and Vitaphone, and King Features published a second collected volume of Believe it or Not! panels. He also appeared in a Vitaphone musical short, Seasons Greetings (1931), with Ruth Etting, Joe Penner, Ted Husing, Thelma White, Ray Collins, and others. After a trip to Asia in 1932, he opened his first museum, the Odditorium, in Chicago in 1933. The concept was a success, and at one point, Odditoriums were in San Diego, Dallas, Cleveland, San Francisco, and New York City. By this point in his life, Ripley had been voted the most popular man in America by The New York Times, and Dartmouth College awarded him an honorary degree.

World travel became impossible during World War II, so Ripley concentrated on charity pursuit. In 1948, the year of the 20th anniversary of the Believe it or Not! cartoon series, the Believe it or Not! radio show drew to a close and was replaced with a Believe it or Not! television series. This was a rather bold move on Ripley's part, because of the small number of Americans with access to television at this early time in the medium's development. He completed only 13 episodes of the series before he became incapacitated by severe health problems. On May 27, 1949, at age 59, he died from a heart attack in New York City. He was buried in his home town of Santa Rosa in the Oddfellows Lawn Cemetery, which is adjacent to the Santa Rosa Rural Cemetery.

The comic strip
Ripley's cartoon series was estimated to have 80 million readers worldwide, and he is said to have received more mail than the President of the United States. He became a wealthy man, with homes in New York and Florida, but he always retained close ties to his home town of Santa Rosa, California, and he made a point of bringing attention to the Church of One Tree, a church built entirely from the wood of a single 300-ft (91.4-m)-tall redwood tree, which stands on the north side of Juilliard Park in downtown Santa Rosa.

Ripley claimed to be able to "prove every statement he made" because he worked with professional fact researcher Norbert Pearlroth, who assembled Believe it or Not! array of odd facts and also verified the small-town claims submitted by readers. Pearlroth spent 52 years as the feature's researcher, finding and verifying unusual facts for Ripley, and after Ripley's death, for the King Features syndicate editors who took over management of the Believe it or Not! panel. Another employee who edited the newspaper cartoon series over the years was Lester Byck. Others who drew the series after Ripley's death include Don Wimmer, Joe Campbell (1946–1956), Art Slogg, Clem Gretter (1941–1949), Carl Dorese, Bob Clarke (1943–1944), Stan Randall, Paul Frehm (1938–1975), who became the panel's full-time artist in 1949, and his brother Walter Frehm (1948–1989).

Legacy
Ripley's ideas and legacy live on in Ripley Entertainment, a company bearing his name and owned since 1985 by the Jim Pattison Group, a privately held company based in Canada. Ripley Entertainment airs national television shows, features publications of oddities, and has holdings in a variety of public attractions, including Ripley's Aquarium, Ripley's Believe it or Not! Museums, Ripley's Haunted Adventure, Ripley's Mini-Golf and Arcade, Ripley's Moving Theater, Ripley's Sightseeing Trains, Guinness World Records Attractions, and Louis Tussaud's Wax Museums.

title: Robert Ripley


text:
Superconducting Super Collider

The Superconducting Super Collider (SSC) (also nicknamed the "Desertron" ) was a particle accelerator complex under construction in the vicinity of Waxahachie, Texas, United States.

Its planned ring circumference was 87.1 km with an energy of 20 TeV per proton and was designed to be the world's largest and most energetic particle accelerator. The laboratory director was Roy Schwitters, a physicist at the University of Texas at Austin. Department of Energy administrator Louis Ianniello served as its first project director, followed by Joe Cipriano, who came to the SSC Project from the Pentagon in May 1990. After 22.5 km (14 mi) of tunnel had been bored and about US$2 billion spent, the project was canceled by the US Congress in 1993.

Proposal and development
The supercollider was formally discussed in the 1984 National Reference Designs Study, which examined the technical and economic feasibility of a machine with the design energy of 20 TeV per proton.

Early in 1983, HEPAP (High-Energy Physics Advisory Panel) formed the New Facilities for the US High-Energy Physics Program subpanel. Led by Stanford University physicist Stanley Wojcicki, and charged with making recommendations “for a forefront United States High Energy Physics Program in the next five to ten years.” the HEPAP subpanel recommended that the US build the Superconducting Super Collider.

Fermilab director and subsequent Nobel physics prizewinner Leon Lederman was a very prominent early supporter – some sources say the architect or proposer – of the Superconducting Super Collider project, as well as a major proponent and advocate throughout its lifetime.

A Central Design Group (CDG) was organized in California at the Lawrence Berkeley Laboratory, which became the gathering place for physicists to come and support the SSC design effort. In the mid-1980s, many leading high-energy physicists, including theorist J. David Jackson of Berkeley, Chris Quigg of Fermilab, Maury Tigner of Cornell, Stanley Wojcicki, as well as Lederman, Chicago’s James Cronin, Harvard theorist Sheldon Glashow, and Roy Schwitters, continued their efforts to promote the Super Collider.

An extensive U.S. Department of Energy review was also done during the mid-1980s. Seventeen shafts were sunk and 23.5 km of tunnel were bored by late 1993.

Partial construction and financial issues

During the design and the first construction stage, a heated debate ensued about the high cost of the project. In 1987, Congress was told the project could be completed for $4.4 billion, and it gained the enthusiastic support of Speaker Jim Wright of nearby Fort Worth, Texas. A recurring argument was the contrast with NASA's contribution to the International Space Station (ISS), a similar dollar amount. Critics of the project (Congressmen representing other US states and scientists working in non-SSC fields who felt the money would be better spent on their own fields) argued that the US could not afford both of them.

Estimates of the additional cost caused by not using existing physical and human infrastructure at Fermilab in Illinois range from $495 million to $3.28 billion.

Leaders hoped to get financial support from Europe, Canada, Japan, Russia, and India. This was hindered by promotion of the project as promoting American superiority. European funding remained at CERN, which was already working on the Large Hadron Collider. India pledged $50 million, but talks with Japan foundered over trade tensions in the automobile industry. A US-Japanese trade mission where SSC funding was supposed to be discussed ended in the George H. W. Bush vomiting incident.

Congress began appropriating annual funding for the project. In 1992, it was opposed by a majority of the House of Representatives (231-181), but was included in the final reconciled budget due to support in the Senate (62-32). Early in 1993, a group supported by funds from project contractors organized a public relations campaign to lobby Congress directly in support of the project. In February, the General Accounting Office reported a $630 million overrun in the $1.25 billion construction budget. By March, the New York Times reported the estimated total cost had grown to $8.4 billion. In June, the non-profit Project on Government Oversight released a draft audit report by the Department of Energy's Inspector General heavily criticizing the Super Collider for its high costs and poor management by officials in charge of it. The Inspector General investigated $500,000 in questionable expenses over three years, including $12,000 for Christmas parties, $25,000 for catered lunches, and $21,000 for the purchase and maintenance of office plants. The report also concluded that there was inadequate documentation for $203 million in project spending, or 40% of the money spent up to that point.

In 1993 U.S. President Bill Clinton tried to prevent the cancellation by asking Congress to continue "to support this important and challenging effort" through completion because "abandoning the SSC at this point would signal that the United States is compromising its position of leadership in basic science".

Cancellation
After $2 billion had been spent ($400 million by the host state of Texas, the rest by the Department of Energy ), the House of Representatives rejected funding on October 19, 1993, and Senate negotiators failed to restore it. Following Rep. Jim Slattery's successful orchestration in the House, President Clinton signed the bill that finally canceled the project on October 30, 1993, stating regret at the "serious loss" for science.

Many factors contributed to the cancellation: rising cost estimates (to $12bn); poor management by physicists and Department of Energy officials; the end of the need to prove the supremacy of American science with the collapse of the Soviet Union and the end of the Cold War; belief that many smaller scientific experiments of equal merit could be funded for the same cost; Congress's desire to generally reduce spending (the United States was running a $255bn budget deficit); the reluctance of Texas Governor Ann Richards; and President Bill Clinton's initial lack of support for a project began during the administrations of Richards's predecessor, Bill Clements, and Clinton's predecessors, Ronald Reagan and George H. W. Bush. The project's cancellation was also eased by opposition from within the scientific community. Prominent condensed matter physicists, such as Philip W. Anderson and Nicolaas Bloembergen, testified before Congress opposing the project. They argued that, although the SSC would certainly conduct high-quality research, it was not the only way to acquire new fundamental knowledge, as some of its supporters claimed, and so was unreasonably expensive. Scientific critics of the SSC pointed out that basic research in other areas, such as condensed matter physics and materials science, was underfunded compared to high energy physics, despite the fact that those fields were more likely to produce applications with technological and economic benefits.

Reactions to the cancellation
Steven Weinberg, a Nobel laureate in Physics, placed the cancellation of the SSC in the context of a bigger national and global socio-economic crisis, including a general crisis in funding for science research and for the provision of adequate education, healthcare, transportation and communication infrastructure, and criminal justice and law enforcement.

Leon Lederman, a leading promoter and advocate of the SSC, wrote a popular science book in the context of the project's last years and loss of congressional support. Published in 1993, The God Particle: If the Universe Is the Answer, What Is the Question? sought to promote awareness of the significance of the scientific work which the SSC would have supported. The book popularized the nickname "the God particle" for the Higgs boson.

The closing of the SSC had adverse consequences for the southern part of the Dallas–Fort Worth Metroplex, contributing to a mild recession especially in those parts of Dallas which lay south of the Trinity River. When the project was canceled, 22.5 km of tunnel and 17 shafts to the surface were already dug, and nearly two billion dollars had already been spent on the massive facility.

Comparison with the Large Hadron Collider
The SSC's planned collision energy of 2 x 20 = 40 TeV was roughly three times that of the 2 x 6.8 = 13.6 TeV (as of 2023) of its European counterpart, the Large Hadron Collider (LHC) at CERN in Geneva. However, the planned luminosity was only one tenth of the design luminosity of the LHC.

Although some claimed that the SSC cost was largely due to the massive civil engineering project of digging a huge tunnel, that was somewhat of a distortion. The tunneling and conventional facility buildout budget was only about ten percent of the total budgeted cost (1.1 billion dollars out of a total cost of 10 billion). The major cost item was the magnets, still in laboratory development phase, consequently with a higher level of uncertainty attached to the final cost. The ring circumference of the LHC is 27 km, compared to the planned 87.1 km of the SSC.

The LHC's advantage in terms of cost was the use of the pre-existing engineering infrastructure and 27 km long cavern of the Large Electron–Positron Collider, and its use of a different, innovative magnet design to bend the higher energy particles into the available tunnel. The LHC eventually cost the equivalent of about 5 billion US dollars to build. The total operating budget of CERN runs to about $1 billion per year. The Large Hadron Collider became operational in August 2008.

In a 2021 interview, Schwitters speculated that, had the project been completed, it would have led to the discovery of the Higgs boson particle 10 years before its eventual discovery in Switzerland and attracted an equivalent number of visitors to North Texas as CERN's 120,000 per year.

Fate of the site

After the project was canceled, the main site was deeded to Ellis County, Texas, and the county tried numerous times to sell the property. The property was sold in August 2006 to an investment group, Collider Data Center, LLC, led by the late J.B. Hunt.

In 2009, Collider Data Center had contracted with GVA Cawley to market the site as a data center. In 2012, chemical company Magnablend bought the property and facilities in the face of some opposition from the local community. The buildings in the facility, which had become prime spots for thieves and drug parties, were renovated and were re-opened in 2013 by Magnablend. The facility makes a range of oil field products for the energy service industry.

In popular culture
In Season 3, Episode 15 of Beavis and Butt-Head, titled "Citizen Butt-Head" which aired on October 18, 1993, the day before Congress cancelled the funding for the Super Collider, an honor student of Highland Highschool is overheard rehearsing his question for President Bill Clinton in which he asks: "Given the budget deficit, do you think the Super Collider is really necessary at this time?"

"Supercollider," a 1993 song by the Boston-based alternative band Tribe, describes the point of view of a scientist hired to help build the (then-uncancelled) project.

John G. Cramer's 1997 hard science fiction novel Einstein's Bridge centers around a fictional version of the Superconducting Super Collider.

On the February 25, 2001, episode of Futurama, entitled “That’s Lobstertainment!,” a robot comedian makes a Super Collider pun and, in tongue-in-cheek fashion, states that a Super Collider was built.

On the March 6, 2002, episode of The West Wing, the supercollider is discussed when Sam Seaborn is helping an old college physics professor get funding to complete the project.

A Hole In Texas is a 2004 novel by Herman Wouk, which describes the adventures of a high-energy physicist following the surprise announcement that a Chinese physicist had discovered the long-sought Higgs boson. Parts of the plot are based on the aborted Superconducting Super Collider project.

On the January 21, 2021, episode of Young Sheldon the supercollider is mentioned when Sheldon Cooper's (Iain Armitage) mentor Dr. John Sturgis (Wallace Shawn) gets a new job there. A subsequent episode on the April 1, 2021, episode shows an exterior shot of the facility with Dr. Sturgis receiving a phone call from Sheldon's grandmother (Annie Potts).

In 2021, the project was cited as a case study of the hypothetical demon of Bureaucratic Chaos, which "blocks good things from happening" at the United States Department of Energy.

title: Superconducting Super Collider


text:
Faustina

Faustina may refer to:

Saints

 * Faustina Kowalska (1905–1938), Polish mystic, "Secretary of Divine Mercy"
 * Saint Faustina and Saint Liberata of Como, 6th-century Italian nuns

Women from the Nerva–Antonine dynasty

 * Rupilia Faustina, a daughter of Vitellia Galeria and the consul Lucius Scribonius Libo Rupilius Frugi Bonus
 * Faustina the Elder (died c. 140), Annia Galeria Faustina Major, daughter of Rupilia Faustina and Marcus Annius Verus; wife of Emperor Antoninus Pius
 * Faustina the Younger (2nd century – 175), Annia Galeria Faustina Minor, daughter of Faustina the Elder and Antoninus Pius; wife of Emperor Marcus Aurelius
 * Annia Cornificia Faustina (123–152), cousin of Faustina to Younger and sister to Marcus Aurelius
 * Annia Fundania Faustina (died 192), cousin of Faustina the Younger and Marcus Aurelius
 * Ummidia Cornificia Faustina (141–182), daughter of Annia Cornificia Faustina and niece of Marcus Aurelius
 * Vitrasia Faustina (died c. 180), daughter of Annia Fundania Faustina
 * Annia Galeria Aurelia Faustina (147 – 2nd century), first-born daughter of Faustina the Younger and Marcus Aurelius
 * Annia Cornificia Faustina Minor (160–212), another sister of Annia Aurelia Galeria Faustina
 * Annia Faustina (daughter of Ummidia Cornificia Faustina) (165 – c. 210), noblewoman of Anatolian Roman descent and a wealthy heiress who lived in the Roman Empire
 * Annia Faustina or Annia Aurelia Faustina, the great, granddaughter of Marcus Aurelius and Faustina the Younger, the third wife of Roman Emperor Elagabalus

Other Roman women

 * Faustina (wife of Constantius II)
 * Faustina Constantia, daughter of Faustina and Constantius
 * Faustina, a hagiographical version of Empress Valeria Maximilla, supposedly converted by St. Catherine of Alexandria

Other people

 * Faustina Agolley, Australian television music presenter
 * Faustina Acheampong, First Lady of the Republic of Ghana
 * Faustina Bordoni (1697–1781), Baroque-era soprano nicknamed "Faustina"
 * Faustina Maratti (c. 1670–1745), Italian Baroque poet and painter
 * Faustina Sáez de Melgar (1834–1895), Spanish writer and journalist
 * Faustina Pignatelli (died 1785), Italian physicist
 * Faustina K. Rehuher-Marugg, Palauan curator and politician
 * Doc Faustina (born 1939), NASCAR driver

Fictional characters

 * Faustina, a character in the 1969 novel A Void

Other uses

 * Faustina (1957 film), a 1957 Spanish comedy
 * Faustina (1968 film), an Italian comedy
 * Faustina (1995 film), a Polish religious drama
 * Faustine (1991 novel), by Emma Tennant
 * Faustina (gastropod), a subgenus of Chilostoma gastropods
 * Faustina (play), a 1948 drama by Paul Goodman

title: Faustina


text:
Carlos Mastronardi

Carlos Mastronardi (1901 – June 5, 1976) was an Argentine journalist, poet, and translator. His works included Luz de provincia, Tierra amanecida (1926), Conocimiento de la noche (1937), and Tratado de la pena. His non-fiction Valéry o la infinitud del método (Valéry, or the infinitude of method) won the Buenos Aires Municipal Prize for Literature (1955). Other important works of non-fiction included Formas de la realidad nacional (Forms of the National Reality, 1961) and Memorias de un Provinciano (Memoirs of a Man from the Provinces, 1967). Some of his journalism was published posthumously as Cuadernos de vivir y pensar (Notebooks of Living and Thinking, 1984).

As a translator, Mastronardi was mainly known for translating the French Symbolist poets into Spanish. As a poet, although identified personally with the avant-garde of his time, he wrote largely in traditional forms rather than free verse, and rejected what he viewed as his contemporaries' excessive use of metaphor.

Born in Gualeguay, Entre Ríos Province, Mastronardi came to Buenos Aires at the age of 19. There he became a member of the Martín Fierro group (also known as the Florida group) and an intimate of Jorge Luis Borges, although they disagreed strongly about questions about aesthetics and poetry. Mastronardi figures as a minor character in Borges's short story Tlön, Uqbar, Orbis Tertius.

Mastronardi led a notoriously nocturnal existence. Writing of Mastronardi in 1986 in the newspaper El País (Madrid), Borges said of Mastronardi that "Like Auguste Dupin ... [ the detective character created by Edgar Allan Poe ] ... at night he went about the streets of Buenos Aires looking for that intellectual stimulus that only can be given by nighttime in a great city."

After a long period in which his work fell into obscurity, Mastronardi's works are being re-published by Argentina's Universidad Nacional del Litoral.

Quotation
"Lyric poetry, for many of its ... [Argentine] ... practitioners, lacks all plan and requires no sacrifice. It allows the writer to follow the path of least resistance: everything consists of letting things be. In contrast, narrative, criticism, and essays (almost uncultivated among us), demand preparatory work and organic development."

title: Carlos Mastronardi


text:
User talk:Warner Mendenhall

Wikipedia Meet up
I invite anybody who likes to come to Shag's Tavern (937) 258-8353 1926 S Smithville Rd Dayton, OH at midnight on Sunday the 21st/Monday the 22nd of March. Meet in the rear, near to the jukebox. Feel free to contact me in regards to specifics. Cheers, User:Sam Spade / Jack

http://en.wikipedia.org/wiki/Wikipedia:Meetup#USA_meet_up

Sam Spade 05:49, 8 Mar 2004 (UTC)

To bad I cant do anymore research :(

title: User talk:Warner Mendenhall


text:
Rick Mears

Rick Ravon Mears (born December 3, 1951) is a retired American race car driver. He is one of four men to win the Indianapolis 500 four times (1979, 1984, 1988, 1991) and is the current record-holder for pole positions in the race with six (1979, 1982, 1986, 1988, 1989, 1991). Mears is also a three-time Indycar series/World Series champion (1979, 1981 and 1982).

Early years
Mears was born in Wichita, Kansas and raised in Bakersfield, California. He began his racing career in off-road racing. In 1976, he was recommended by a representative of Bill Simpson's helmet company, and Simpson gave him a ride at the USAC Champ Car's California 500 on an old Eagle-Offenhauser, finishing 8th. Simpson then sold the car to Art Sugai, on condition that Mears would continue driving it. In mid 1977 he switched to Theodore Racing.

His speed attracted the attention of Roger Penske. Although at the time Penske Racing had the services of Mario Andretti and Tom Sneva, Andretti was also racing in Formula One with Lotus, and Penske wanted another young driver who would focus exclusively on American racing. For 1978, Mears was offered a part-time ride in nine of the 18 championship races, filling in when Andretti was overseas. The arrangement also included a ride at the Indianapolis 500.

In his rookie appearance at Indy, Mears qualified on the front row and was the first rookie to qualify over 200 mph. When the race began, Mears discovered his helmet was not strapped on tight enough and he had to pit to get it safely secured. He did not lead a lap and retired at 104 laps with a blown engine. He ended up sharing "Rookie of the Year" honors with Larry Rice. Two weeks later, the Rex Mays Classic at Milwaukee, he won his first race. He added another win a month later at Atlanta and rounded off the year with his first road course win at Brands Hatch. Because of his terrific showing as a rookie, Mears was elevated to full-time status for 1979 after teammate and series champion Tom Sneva and Penske parted company.

1979
In 1979 the National Championship sanction changed from the USAC to CART. At Indianapolis he won his first "500", staying at the front of the field, taking advantage when Bobby Unser fell out of contention with mechanical trouble. Three wins and four second places in the eleven CART-eligible races won Mears his first championship. His worst finish in the season was seventh in Trenton's second heat.

1980
In 1980 the ground effect Chaparral was technologically more advanced than the other chassis, and Johnny Rutherford drove it to his 3rd Indianapolis 500 win, going on to dominate the season. Mears finished in fourth place in the points with one win, scored at Mexico City.

In 1980 Mears was offered a Formula One test with Brabham by then team boss Bernie Eccelstone. Mears took interest in the test largely because of the ongoing split between CART and USAC and wanted other options in case CART fell apart. Mears tested with Brabham twice, once at Paul Ricard and once at Riverside. After adjusting his driving style to the Brabham BT49 Mears posted lap times within half a second of future three time Formula One champion and then Brabham driver Nelson Piquet at the first test. During the second test Mears posted lap times faster than Piquet's. Piquet was so impressed with Mears' driving and enjoyed their time spent together so much that he endorsed bringing Mears on as a second driver. Eccelstone offered Mears a contract with Brabham that Mears ultimately declined. Mears would later say in his memoir that although he felt that Brabham was a strong team and that he had the skill to compete for wins in Formula One he was unsure about moving to Europe and was still interested in oval racing as the main reasons for declining Eccelstone's offer.

1981–1982
The 1981 and 1982 seasons saw two more championships for Mears. Despite facial burns during a pit fire in the 1981 Indianapolis 500, Mears' ten race victories in the two-year span were enough for another two Indycar championship titles. At the 1982 Indianapolis 500 he came within 0.16 of a second of adding a second Indy win. With less than 20 laps to go, during Mears' final pit stop, the crew filled the entire tank rather than giving him only the amount he needed to finish. The delay left him more than 11 seconds behind Gordon Johncock. Mears made up the difference when Johncock suffered handling problems, but failed to secure the win. The photo finish stood for 10 years as the closest finish to an Indy 500. The photo-finish also muffled out the controversial pace-lap crash with teammate Kevin Cogan who appeared to have spun out for no apparent reason; fellow drivers such as Gordon Johncock, Johnny Rutherford, and Bobby Unser, charged Mears with causing the crash by bringing the field down at a slow pace.

1983–1984
For 1983 the Penske team acquired the Pennzoil sponsorship with its yellow paint scheme. Teammate Al Unser took that year's title. The team switched to the March chassis for the 1984 Indianapolis 500 after the Penske chassis proved unsuccessful in the first two races of the year. Mears scored his second Indy win that May but suffered severe leg injuries later in the year in a crash at Sanair Super Speedway. The March chassis, like most contemporary open-wheel racing cars, sat the driver far forward in the nose, with little protection for the legs and feet.

1985–1987
After the Sanair crash, Mears was slowed by the injuries to his right foot that affected him throughout the remainder of his career. Over the next three seasons, he won only two races. He completed a comeback from his injuries by winning the 1985 Pocono 500. In 1986, he won the pole position for the Indianapolis 500, but finished 3rd. He also won the 1987 Pocono 500.

1988–1990
In 1988, after several years using the March chassis, the Penske team utilized a new car, the PC-17, with a Chevrolet racing engine. Mears used the new car to win the Indianapolis 500. A year later, he took a record-setting fifth pole position at Indy, but retired from the race with mechanical problems. Emerson Fittipaldi took the 500 and also beat Mears to the Championship in the last race at Laguna Seca Raceway, despite Mears winning that race. Also, that last race of 1989 set Mears apart from all other Indycar racers as he broke a tie with Bobby Rahal for race wins and became the most successful Indycar racer of the 1980s. In his winner's circle interview, when asked about breaking his road course dry spell when his specialty has been ovals through the years, he replied to Jack Arute, "Well, I guess there is hope for us old circle track drivers after all."

Fittipaldi joined Mears at Penske for 1990, but the year belonged to Al Unser Jr., who scored six wins. 1990 was Mears' last in the Pennzoil paint scheme as Marlboro took over as sponsor of the team, and Jim Hall re-entered Indycar.

1991–1992
In 1991 during a practice session Mears hit the wall at Indianapolis for the first time in his career. The next day, he climbed into his backup car and claimed his record 6th career pole position. Twenty laps from the end of the 500, it looked like Mears was set to be the runner-up behind Michael Andretti. However, when a subsequent yellow flag period erased Andretti's 15-second lead, Mears gained the lead as Andretti opted to pit for fuel. It was a short-lived lead, as Andretti passed Mears around the outside into the first turn. A lap later Mears regained the lead, using the same move Andretti had. Turning up his turbocharger, he then pulled away to win a fourth Indy 500, becoming the third driver to do so. In August 1991, in the Michigan 500, he won his last race.

At the 1992 Indianapolis 500 Mears broke a wrist in a crash during practice and then crashed out of the race for the first time in his career as he could not avoid Jim Crawford's spinning car in turn 1. He raced only four more times in 1992 and then announced his retirement from racing at the Penske team's Christmas party. No one except Penske himself and Rick's wife, Chris, knew of his plans to retire. He had just turned 41 years old.

As of 2023, Rick Mears continues to work as a consultant and spotter for Penske Racing, the team with which he won all of his Indycar races. He has acted as a mentor for Penske drivers Helio Castroneves, Will Power, and Scott McLaughlin.

Personal life
Mears is the brother of Roger Mears, father of off-road and open-wheel racer Clint Mears, and the uncle of former NASCAR Cup Series driver Casey Mears. His marriage to his first wife Dina ended in divorce in 1983. He married Chris Bowen in 1986 whom he divorced in 2002.

Awards

 * In 1997, he was inducted into the International Motorsports Hall of Fame.
 * Mears was inducted into the Indianapolis Motor Speedway Hall of Fame in 1998.
 * He was inducted in the Motorsports Hall of Fame of America in 1998.
 * Inducted into Team Penske Hall of Fame on May 25, 2017

USAC
(key) (Races in bold indicate pole position)

CART Series
(key) (Races in bold indicate pole position)

International Race of Champions
(key) ( Bold – Pole position. * – Most laps led. )

title: Rick Mears


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Karl Davydov

Karl Yulievich Davydov (Карл Юльевич Давидов; 15 March 1838 – 26 February 1889) was a Russian cellist, described by Pyotr Ilyich Tchaikovsky as the "czar of cellists". He was also a composer, mainly for the cello. His name also appears in various different spellings: Davydov, Davidoff, Davidov, and more, with his first name sometimes written as Charles or Carl.

Biography
Davydov was the son of a Jewish physician and amateur violinist, Yuly Petrovich Davidhoff from Courland Governorate. His elder brother August Davidov was a noted mathematician and educator, and his nephew Alexei Davidov also became cellist and composer and also a businessman.

In his youth Davydov studied mathematics at St. Petersburg University, and then pursued a career as a composer, studying with Moritz Hauptmann at the Leipzig Conservatory. He became a full-time cello soloist in 1850 while continuing to compose. He took a post as a professor of cello at the St Petersburg Conservatory in 1863, and subsequently became director in 1878. In 1886 scandal forced him from his position, and Anton Rubinstein took the helm. He had many students, including Aleksandr Verzhbilovich.

He intended to write an opera on the subject of Mazeppa. Viktor Burenin wrote a libretto for this purpose in 1880, but when Davydov proved unable to find the time to compose, Burenin offered the libretto to Tchaikovsky. Although closely associated with Tchaikovsky, Karl Davydov was not related to the Princes Davydov, Russian Orthodox, into which Tchaikovsky's sister Alexandra married.

Davydov was well-connected with a great number of the top-tier composers, musicians and nobility. In 1870 Count Wilhorsky, a patron of the arts, presented Davydov with a Stradivarius cello constructed in 1712. This cello, now known as the Davidov Stradivarius, was owned by Jacqueline du Pré until her death and is currently on loan to cellist Yo-Yo Ma. Several composers dedicated works to him, notably Tchaikovsy's Cappricio Italien and Anton Arensky's first piano trio.

Davydov went on to write his still-popular "cello school" book of etudes and technique, completed in 1888, taking the physical limitations into considerations for advancing the possibilities in both the bow hand and playing in the high registers. Davydov died in Moscow on 26 February 1889.

In 2019 a Moscow regional cello competition was established in his name.

Cello transcriptions
Davydov transcribed and arranged Chopin's solo piano works for violoncello and piano accompaniment. Transcription albums of Walzer and Mazurkas published by Breitkopf & Härtel. Another transcription album is a selection of Nocturnes and others solo piano works published by Edition Peters.

Selected works

 * Opus 5, Cello Concerto No. 1 in B minor (1859)
 * Opus 6, Souvenir de Zarizino: 2 salon pieces (Nocturne – Mazurka) for cello and piano
 * Opus 7, Fantasie from a Russian folk song for cello and orchestra
 * Opus 9, 3 Pièces caractéristiques for cello and piano
 * Opus 11, Concert Allegro in A minor for cello and orchestra or cello and piano
 * Opus 14, Cello Concerto No. 2 in A minor (1863)(1860?)
 * Opus 16, 3 Salon pieces (Mondnacht, Lied, Märchen) for cello and piano
 * Opus 17, Souvenirs d'Oranienbaum (Adian – Barcarolle)
 * Opus 18, Cello Concerto No. 3 in D major (1868)
 * Opus 20, 4 Pieces for Cello and Piano
 * No. 1, Sonntag Morgen (Sunday Morning)
 * No. 2, Am Springbrunnen (At the Fountain)
 * No. 3, An der Wiege
 * No. 4, Abenddämmerung
 * Opus 23, Romance sans Paroles in G major
 * Opus 25, Ballade for cello and orchestra or piano in G major (1875)
 * Opus 30, 3 salon pieces
 * Opus 31, Cello Concerto No. 4 in E minor (1878)
 * Opus 35, String Sextet
 * Opus 37, Suite pour l'orchestre (Suite for Orchestra)
 * I. Scéne rustique
 * II. Quasi valse
 * III. Scherzo
 * IV. Petite romance
 * V. Marche
 * "Poltawa", Opera after Pushkin (1876, unfinished)
 * Hymn for 10 Celli and Percussion
 * Opus 40, Quintet for Piano and Strings in G minor (1884)

title: Karl Davydov


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Faustina the Elder

Annia Galeria Faustina the Elder, sometimes referred to as Faustina I or Faustina Major (c. 100 – late October 140),  was a Roman empress and wife of the Roman emperor Antoninus Pius. The emperor Marcus Aurelius was her nephew and later became her adopted son, along with Emperor Lucius Verus. She died early in the principate of Antoninus Pius, but continued to be prominently commemorated as a diva, posthumously playing a prominent symbolic role during his reign.

Early life
Faustina was the only known daughter of consul and prefect Marcus Annius Verus and Rupilia Faustina. Her brothers were consul Marcus Annius Libo and praetor Marcus Annius Verus. Her maternal aunts were Roman Empress Vibia Sabina and Matidia Minor. Her paternal grandfather was named Marcus Annius Verus, like her father, while her maternal grandparents were suffect consul Lucius Scribonius Libo Rupilius Frugi Bonus and possibly Vitellia. Faustina was born and raised in Rome.

While a private citizen, she married Antoninus Pius between 110 and 115. Faustina bore four children with Pius: two sons and two daughters. These were:
 * Marcus Aurelius Fulvius Antoninus (died before 138); his sepulchral inscription has been found at the Mausoleum of Hadrian in Rome.
 * Marcus Galerius Aurelius Antoninus (died before 138); his sepulchral inscription has been found at the Mausoleum of Hadrian in Rome. He is commemorated by a high-quality series of bronze coins, possibly struck at Rome, though their language is Greek.
 * Aurelia Fadilla (died in 135); she married Aelius Lamia Silvanus or Syllanus. She appears to have had no children with her husband and her sepulchral inscription has been found in Italy.
 * Annia Galeria Faustina Minor or Faustina the Younger (between 125–130 to 175), a future Roman Empress; she married her maternal cousin, future Roman Emperor Marcus Aurelius. She was the only child who survived to see Antoninus and Faustina elevated to the imperial rank.

According to the unreliable Historia Augusta, there were rumours while Antoninus was proconsul of Asia that Faustina conducted herself with "excessive frankness and levity".

Empress

On July 10, 138, her uncle, the emperor Hadrian, died and her husband became the new emperor, as Antoninus was Hadrian's adopted son and heir. Faustina became Roman Empress and the Senate accorded her the title of Augusta. As empress, Faustina was well respected and was renowned for her beauty and wisdom. Throughout her life, as a private citizen and as empress, Faustina was involved in assisting charities for the poor and sponsoring and assisting in the education of Roman children, particularly girls. A letter between Fronto and Antoninus Pius has sometimes been taken as an index of the latter's devotion to her.

After Antoninus Pius' accession to the principate, the couple never left Italy; instead, they divided their time between Rome, Antoninus' favourite estate at Lorium, and other properties at Lanuvium, Tusculum, and Signia.

Faustina's personal style was evidently much admired and emulated. Her distinctive hairstyle, consisting of braids pulled back in a bun behind or on top of her head, was imitated for two or three generations in the Roman world.

Several provincial groups chose to honour her while she was empress: a company of couriers in Ephesus named themselves after her, while a company of clapper-players in Puteoli dedicated an altar to her in her lifetime.

Death and legacy

Faustina died near Rome in 140, perhaps at Antoninus Pius's estate at Lorium. Antoninus was devastated at Faustina's death and took several steps to honor her memory. He had the Senate deify her (her apotheosis was portrayed on an honorary column) and dedicate the Temple of Faustina to her in the Roman Forum. Because of this, Faustina was the first Roman empress with a permanent presence in the Forum Romanum. The Senate authorized gold and silver statues of her, including an image to appear in the circus, where it might be displayed in a carpentum (a kind of covered wagon) or currus elephantorum (a cart drawn by elephants). Antoninus also ordered various coins with her portrait struck, inscribed DIVA FAVSTINA ("Divine Faustina") and elaborately decorated. He also established a charity called Puellae Faustinianae ("Girls of Faustina") to assist orphaned Roman girls and created a new alimenta (see Grain supply to the city of Rome). Her remains were interred in the Mausoleum of Hadrian. Certain cities struck coin issues in honour of the "divine Faustina" (ΘΕΑ ΦΑΥϹΤΕΙΝΑ); the most notable such cities were Delphi, Alexandria, Bostra, and Nicopolis. Martin Beckmann suggests that the coins of Nicopolis might have been minted at Rome and given out as imperial largesse at the Actian Games. The coins issued in the wake of Faustina's funeral illustrate her elaborate funeral pyre, which may have influenced the design of later private mausolea; the deities Pietas and Aeternitas, among others; and an eagle (or less often a winged genius) bearing a figure aloft, with the legend CONSECRATIO (i.e. Faustina's ascension into heaven). Coins of Faustina were sometimes incorporated into jewellery and worn as amulets.

The posthumous cult of Faustina was exceptionally widespread, and Faustina's image continued to be omnipresent throughout Antoninus Pius' principate. A colossal marble head, believed to be that of Faustina and discovered in 2008, figured as one of several monumental imperial statues at the ancient site of Sagalassos in today's Turkey. In Olympia, Herodes Atticus dedicated a nymphaeum that displayed statues of Faustina and other Antonines as well as his own ancestors. Faustina also appears on the Parthian Monument at Ephesus commemorating members of the imperial family. Bergmann and Watson have characterized the commemoration of Faustina as central to Antoninus Pius' political persona. One larger-than-life statue, discovered in situ near the Termini railway station at Rome, appears to depict Faustina as Concordia, with a patera and cornucopia; it would have been displayed alongside statues of Diana Lucifera and Apollo-Sol in baths privately owned but available to the public.

Antoninus and Faustina were officially held up as such exemplars of conjugal harmony that newlyweds were directed to pray at an altar of Antoninus and Faustina that they might live up to their example. This was evidently the case in Ostia, and probably so in Rome.

The Temple of Faustina is thought to have been dedicated in 144. It is a grand hexastyle structure with Corinthian columns, possibly designed originally to be a temple of Ceres. Depictions on coins appear to show a cult image of Faustina seated on a throne and holding a tall staff in her left hand. Faustina's portrait on coins from this period is often crowned as well as veiled, which may also recall a feature of Faustina's cult image from the temple.

The deified Faustina was associated particularly closely with Ceres, who featured prominently on coins of Faustina; for some years, the torch-bearing Ceres was the dominant motif in her gold coinage. Herodes Atticus venerated Faustina as the “new Demeter” (the Greek equivalent of Ceres) at a private sanctuary he established outside Rome, now the church of Sant'Urbano. In addition to Ceres, Vesta and Juno feature prominently in Faustina's coinage. She was also associated with the Magna Mater and at Cyrene with Isis; at Sardis she was worshipped conjointly with Artemis.

Ten years after Faustina's death, a new commemorative coinage was introduced, featuring the legend Aeternitas ('eternity'); such coins may have been introduced to be distributed at a public ceremony in her memory.

After Antoninus Pius' death, his adoptive sons and successors Marcus Aurelius and Lucius Verus erected the Column of Antoninus Pius, which dramatically depicted Antoninus and Faustina being elevated heavenward together on the back of a winged figure.

Marcus Aurelius also built a Temple of Faustina at Elefsina in Greece.

Faustina continued to be commemorated in certain Renaissance depictions as a “model wife”.

title: Faustina the Elder


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Linaria

Linaria is a genus of almost 200 species of flowering plants, one of several related groups commonly called toadflax. They are annuals and herbaceous perennials, and the largest genus in the Antirrhineae tribe of the plantain family Plantaginaceae.

Taxonomy
Linaria was traditionally placed in the family Scrophulariaceae. Phylogenetic analysis has now placed it in the vastly expanded family Plantaginaceae.

Closely related genera include Nuttallanthus (American toadflaxes, recently split from Linaria), Antirrhinum (snapdragons) and Cymbalaria (ivy-leaved toadflaxes).

Cultivation
Several Linaria species are cultivated as garden plants, and some are regarded as having a weedy habit.

 * Common toadflax or butter-and-eggs (Linaria vulgaris), a European species which is widely introduced elsewhere and grows as a common weed in some areas.
 * Broomleaf toadflax or Dalmatian toadflax (Linaria genistifolia, syn. L. dalmatica), a native of southeast Europe that has become a weed in parts of North America.
 * Purple toadflax (Linaria purpurea), a species native to the Mediterranean region grown as a garden plant for its dark purple or pink flowers. The version with purple flowers can be mistaken for lavender. Spreads readily.
 * Pale toadflax (Linaria repens), a species from western Europe similar to L. purpurea, but with paler flowers.
 * Alpine toadflax (Linaria alpina), purple flowers with orange (or purple) lobes in the center.
 * Moroccan toadflax (Linaria maroccana), the flower has five lobes arranged into two lips with a spur at the end, often purple with white.

Species
The following species are recognised in the genus Linaria:

 * Linaria accitensis L.Sáez, Juan, M.B.Crespo, F.B.Navarro, J.Peñas & Roquet
 * Linaria acutiloba Fisch.
 * Linaria aeruginea (Gouan) Cav.
 * Linaria afghanica Podlech & Iranshahr
 * Linaria alaica Junussov
 * Linaria albifrons (Sm.) Spreng.
 * Linaria algarviana Chav.
 * Linaria alpina (L.) Mill.
 * Linaria altaica Fisch.
 * Linaria amethystea (Vent.) Hoffmanns. & Link
 * Linaria amoi Campo ex Amo
 * Linaria angustissima (Loisel.) Borbás
 * Linaria antilibanotica Rech.f.
 * Linaria arcusangeli Atzei & Camarda
 * Linaria arenaria DC.
 * Linaria arenicola Pau & Font Quer
 * Linaria argillicola Juan, Blanca, Cueto, J.Fuentes & L.Sáez
 * Linaria armeniaca Chav.
 * Linaria arvensis (L.) Desf.
 * Linaria atlantica Boiss. & Reut.
 * Linaria azerbaijanensis Hamdi & Assadi
 * Linaria badachschanica Junussov
 * Linaria badalii Willk.
 * Linaria bamianica Patzak
 * Linaria becerrae Blanca, Cueto & J.Fuentes
 * Linaria bessarabica Kotov
 * Linaria biebersteinii Besser
 * Linaria bipartita (Vent.) Willd.
 * Linaria bipunctata (L.) Dum.Cours.
 * Linaria bordiana Santa & Simonn.
 * Linaria boushehrensis Hamdi & Assadi
 * Linaria brachyphylla Delip.
 * Linaria bubanii Font Quer
 * Linaria bungei Kuprian.
 * Linaria buriatica Turcz. ex Ledeb.
 * Linaria caesia (Lag. ex Pers.) F.Dietr.
 * Linaria capraria Moris & De Not.
 * Linaria cavanillesii Chav.
 * Linaria chalepensis (L.) Mill.
 * Linaria clementei Haens. ex Boiss.
 * Linaria confertiflora Benth.
 * Linaria corifolia Desf.
 * Linaria × cornubiensis Druce
 * Linaria cossoniana Braun-Blanq. & Maire
 * Linaria cossonii Bonnet & Barratte
 * Linaria cretacea Fisch. ex Spreng.
 * Linaria dalmatica (L.) Mill.
 * Linaria damascena Boiss. & Gaill.
 * Linaria decipiens Batt.
 * Linaria depauperata Leresche ex Lange
 * Linaria diffusa Hoffmanns. & Link
 * Linaria dissita Pomel
 * Linaria × dominii Druce
 * Linaria dumanii A.Duran & Menemen
 * Linaria elegans Cav.
 * Linaria elymaitica (Boiss.) Kuprian.
 * Linaria fallax Coss. ex Batt.
 * Linaria farsensis Hamdi & Assadi
 * Linaria fastigiata Chav.
 * Linaria faucicola Leresche & Levier
 * Linaria fedorovii Kamelin
 * Linaria ficalhoana Rouy
 * Linaria flava (Poir.) Desf.
 * Linaria genistifolia (L.) Mill.
 * Linaria gharbensis Batt. & Pit.
 * Linaria glacialis Boiss.
 * Linaria glauca (L.) Cav.
 * Linaria golestanensis Hamdi & Assadi
 * Linaria grandiflora Desf.
 * Linaria griffithii Benth.
 * Linaria grjunerae Knjaz.
 * Linaria guilanensis Hamdi & Assadi
 * Linaria haelava (Forssk.) Delile
 * Linaria hepatica Bunge
 * Linaria heratensis Podlech & Iranshahr
 * Linaria hirta (L.) Moench
 * Linaria hohenackeri Tzvelev
 * Linaria huteri Lange
 * Linaria × hybrida Schur
 * Linaria iconia Boiss. & Heldr.
 * Linaria ikonnikovii Stasiak
 * Linaria imzica Gómiz
 * Linaria incarnata (Vent.) Spreng.
 * Linaria incompleta Kuprian.
 * Linaria intricata Coincy
 * Linaria iranica Hamdi & Assadi
 * Linaria × jalancina Gómez Nav., R.Roselló, A.Guillén, P.P.Ferrer, E.Laguna & Per
 * Linaria japonica Miq.
 * Linaria jaxartica Levichev
 * Linaria joppensis Bornm.
 * Linaria kavirensis Hamdi & Assadi
 * Linaria khalkhalensis Hamdi & Assadi
 * Linaria khorasanensis Hamdi & Assadi
 * Linaria × kocianovichii Asch.
 * Linaria kokanica Regel
 * Linaria kulabensis B.Fedtsch.
 * Linaria kurdica Boiss. & Hohen.
 * Linaria latifolia Desf.
 * Linaria laxiflora Desf.
 * Linaria leptoceras Kuprian.
 * Linaria lineolata Boiss.
 * Linaria loeselii Schweigg.
 * Linaria longicalcarata D.Y.Hong
 * Linaria macrophylla Kuprian.
 * Linaria macroura (M.Bieb.) M.Bieb.
 * Linaria maroccana Hook.f.
 * Linaria maymanica Wendelbo
 * Linaria mazandaranensis Hamdi & Assadi
 * Linaria melampyroides Kuprian.
 * Linaria melanogramma Rech.f., Aellen & Esfand.
 * Linaria meyeri Kuprian.
 * Linaria michauxii Chav.
 * Linaria micrantha (Cav.) Hoffmanns. & Link
 * Linaria microsepala A.Kern.
 * Linaria multicaulis (L.) Mill.
 * Linaria munbyana Boiss. & Reut.
 * Linaria musilii Velen.
 * Linaria nachitschevanica Tzvelev
 * Linaria nigricans Lange
 * Linaria nivea Boiss. & Reut.
 * Linaria nurensis Boiss. & Hausskn.
 * Linaria nuristanica Patzak
 * Linaria oblongifolia (Boiss.) Boiss. & Reut.
 * Linaria odora (M.Bieb.) Fisch.
 * Linaria oligantha Lange
 * Linaria × oligotricha Borbás
 * Linaria onubensis Pau
 * Linaria orbensis Carretero & Boira
 * Linaria ordubadica Tzvelev
 * Linaria pamirica (Junussov) Stasiak
 * Linaria paradoxa Murb.
 * Linaria parviracemosa D.A.Sutton
 * Linaria pedicellata Kuprian.
 * Linaria pedunculata (L.) Chaz.
 * Linaria pelisseriana (L.) Mill.
 * Linaria peloponnesiaca Boiss. & Heldr.
 * Linaria peltieri Batt.
 * Linaria pinifolia (Poir.) Thell.
 * Linaria platycalyx Boiss.
 * Linaria polygalifolia Hoffmanns. & Link
 * Linaria popovii Kuprian.
 * Linaria propinqua Boiss. & Reut.
 * Linaria pseudolaxiflora Lojac.
 * Linaria pseudoviscosa Murb.
 * Linaria purpurea (L.) Mill.
 * Linaria pyramidalis (Vent.) F.Dietr.
 * Linaria qartobensis Blanca, Cueto, J.Fuentes, L.Sáez & Tarifa
 * Linaria quasisessilis Levichev
 * Linaria reflexa (L.) Desf.
 * Linaria remotiflora Patzak
 * Linaria repens (L.) Mill.
 * Linaria ricardoi Cout.
 * Linaria riffea Pau
 * Linaria × rocheri P.Fourn.
 * Linaria rubioides Vis. & Pancic
 * Linaria sabulosa Czern. ex Klokov
 * Linaria salangensis Podlech & Iranshahr
 * Linaria salzmannii Boiss.
 * Linaria saposhnikovii Nikitina
 * Linaria saturejoides Boiss.
 * Linaria saxatilis (L.) Chaz.
 * Linaria schelkownikowii Schischk.
 * Linaria schirvanica Fomin
 * Linaria semialata D.López, Sánchez-Gómez, J.F.Jiménez, J.B.Vera & Güemes
 * Linaria × sepium G.J.Allman
 * Linaria sessilis Kuprian.
 * Linaria simplex Desf.
 * Linaria spartea (L.) Chaz.
 * Linaria striatella Kuprian.
 * Linaria supina (L.) Chaz.
 * Linaria tarhunensis Pamp.
 * Linaria tenuis (Viv.) Spreng.
 * Linaria thibetica Franch.
 * Linaria thymifolia (Vahl) DC.
 * Linaria tingitana Boiss. & Reut.
 * Linaria tonzigii Lona
 * Linaria triornithophora (L.) Cav.
 * Linaria triphylla (L.) Mill.
 * Linaria tristis (L.) Mill.
 * Linaria tursica Valdés & Cabezudo
 * Linaria unaiensis Patzak
 * Linaria × valdesiana Socorro & Aroza
 * Linaria venosa Lindl.
 * Linaria ventricosa Coss. & Balansa
 * Linaria veratrifolia Patzak
 * Linaria verticillata Boiss.
 * Linaria virgata (Poir.) Desf.
 * Linaria viscosa (L.) Dum.Cours.
 * Linaria volgensis Rakov & Tzvelev
 * Linaria vulgaris Mill.
 * Linaria warionis Pomel
 * Linaria weilleri Emb. & Maire
 * Linaria yunnanensis W.W.Sm.
 * Linaria yusufeliensis A.Galán, Makbul & Hamzaoglu
 * Linaria × zaborskiana Emb.
 * Linaria zaissanica Semiotr.

Etymology
The members of this genus are known in English as toadflax, a name shared with several related genera. The 'toad' in toadflax may relate to the plants having historically been used to treat bubonic plague, a false link having been drawn between the words 'bubo' and 'Bufo'. The scientific name Linaria means "resembling linum" (flax), which the foliage of some species superficially resembles.

Distribution and habitat
The genus is native to temperate regions of Europe, northern Africa and Asia, with the highest species diversity in the Mediterranean region.

Ecology
Some Linaria are regarded as noxious weeds. They are likely toxic to livestock, but ruminants generally avoid them.

Chemical composition
Linaria species are rich in alkaloids, iridoids, terpenes, phenolic acids and flavonoids.

Vasicine, Vasicinone, 7-hyrdoxyvasicine, Linarinic acid, Choline, Linavuline, Luteolin, Acacetin, Apigenin, Chrysin, Quercetin, Myricetin, Linarioside, Aucubin, Linaride, Iridolinaroside A-D, Iridolinarin A-C are some compounds found in plants of this genus.

Uses
Toadflaxes are used as food plants by the larvae of some Lepidoptera species, including the mouse moth (Amphipyra tragopoginis) and the common buckeye (Junonia coenia).

Traditional medicine
Linaria vulgaris has been used as a medicinal herb.

title: Linaria