All this site (text, images, databases) is copyright by Massimo Faraggi, released with CC BY-NC-ND 3.0 license.
Since 1997 - that is, last century! - maxbeer.org has been reporting the craft beer scene, then at the beginning, with an always updated guide of all the microbreweries in Italy, together with the best beershops and beer bars. With the years - and with the ever increasing number of new breweries - the task of updating the Guide without delays become more difficult; in the meantime other sites specialized with good result on this task. So I decided to give up the updates, only giving in this section some links (just the main ones) for the details. The old Beer Guide (updated up to about 2006) is still available in the Vintage section, as an "historical" document.
Mondobirra Used to be the main resource about microbreweries, now it is less updated than microbirrifici.org but richer in other informations: photos, interviews, videos, news etc.
Cronache di Birra Among the many beer blogs, certainly the best known, most visited, updated and interesting.
Guida alle birre d'Italia 2011 by Slowfood. Most of the existing microbreweries, with full descriptions of each one and reviews and ratings of each beer. The next edition (2013) will be out in 2012.
Unionbirrai is the associations gathering (since last century) many italian microbreweries, and also generally promotes craft beer culture.
MoBI, Movimento Birrario Italiano (Italian Beer Movement) is the italian national craft beer consumers and homebrewing association.
In the MoBI's (and Unionbirrai's) website you can find links an references of other local beer consumers associations.
The "Vintage" Guide: the old Guide on this site (see above), no more updated but still with plenty of informations.


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Aboriginal & Torres Strait Islander art
Return to collections
Aboriginal and Torres Strait Islander peoples have existed on the continent of Australia for tens of thousands of years. Their art and traditions are among the oldest and richest in human history.
The designs, patterns and stories were taught to Indigenous Australians by the Ancestors and are reinforced and replicated through ritual, dance, song, body painting, rock engravings and paintings, and on domestic and ritual objects. Aboriginal and Torres Strait Islander art is as alive today as it was thousands of years ago. As in the ancient past, the art is inseparable from everyday life.
The art of contemporary Indigenous Australians takes many forms. Despite significant change and diversity, the art retains an underlying unity of inspiration—the land and the peoples' relationships with it. It is simultaneously connected to the past and engaged with the present, engaging with the world through actions which are lively, positive, political, social and creative.
The Aboriginal and Torres Strait Islander art collection at the National Gallery of Australia comprises over 7500 works and is the largest in the world. These new gallery spaces allow much more of the collection to be seen with each one specifically designed for a different geographic region or aspect of Indigenous art and, where possible, paintings and sculptures are illuminated overhead by natural daylight, akin to the light in which the works were created.
This dedicated display of Aboriginal and Torres Strait Islander art highlights the diversity, richness and excellence of the collection.
The Aboriginal Memorial
19th Century Objects
Early Western Desert Paintings 1971-1974
Desert Painting from 1975
Hermannsburg School
Early Bark Paintings and Sculpture - pre 1980
Bark Paintings - post 1980, North Queensland and Tiwi Islands

redpajama_set_name: RedPajamaCommonCrawl


text:
APR 18 - MAY 23, 2018 \\ NEW YORK, NY
Location/Dates
Cost/Register
SING (G&S)
CHORUSES
IN PUBLIC!
\\ a fundraiser for House of Murgatroyd Entertainment (H.O.M.E.) \\
NINA LAINVILLE, conductor
Nina Lainville is a Franco-British actress, singer and conductor. She has lived and worked in Paris (France) and London (UK) until moving to New York, NY in 2017.
After studying musicology at the Université Paris VIII, Classical singing at Guildhall School of Music and Drama in London and acting at London Method acting, Nina launched a very eclectic (and a little eccentric) stage performance career as a singer and an actress. Alongside her stage career, Nina is passionate about conducting choirs and believes strongly in the cathartic effects of singing in a group for individuals and their communities.
She has worked with varied choirs from elementary school children, people with physical and mental disabilities, LIPS Choir, Women Sing East, Tenovus Cancer Choir Sing with Us, choirs for people affected by cancer and many community choirs. Nina has sung with the London Philharmonic Choir (touring South East Asia) and has recently join the Canticum Novum Singers in NYC.
Nina is looking forward to immersing herself in the fantastic world of Gilbert and Sullivan's music and having fun singing with the whole group.
DAVID MACALUSO, producer
David Macaluso David Macaluso was an original cast member of the Drama Desk - nominated production of "Pinafore!" where he simultaneously played two lead roles, Sir. Joseph and Buttercup (Vortex Theater). Variety stated, " It's Macaluso that makes this saucy ship a beauty!" As a principal performer with the New York Gilbert and Sullivan Players for over 15 years he was honored to receive the Isaac Asimov Award for Artistic Excellence and was recently managing producer, performer and co-director of the sold out Cox & Box. As a performer he has appeared to critical acclaim Off Broadway at The Signature Theater, Dodger Stages, New York City Center, Symphony Space, Weill Recital Hall at Carnegie Hall, and regionally with Washington Symphony, Opera Columbus and Wolf Trap in Washington D.C. New works include a live broadcast of BOUNCE: A Basketball Opera on WQXR, and The Emperor and The Queen with HERE Arts, workshops of Miracolo-A New Musical, WARSAW, and The Pirates of Finance at The New York Music Theatre Festival. Besides the works of G&S, David has performed in many musicals and operettas, standouts being Molina in "Kiss of the Spiderwoman", Seymour in "Little Shop of Horrors", Motel in "Fiddler" and Dr. Falke "Die Fledermaus". The New York Times praised David's performance in Ruddigore as being "vividly sung and enacted." In The Mikado, with NYGASP, BroadwayWorld raved of his "exuberant showmanship and handling Gilbert's verbal wit with crackling dexterity," and was deemed "the evening's energetic comic engine." Of the acclaimed House of Murgatroyd at the International G&S Festival in England, Seen and Heard International commended both David's "velvety rich baritone" for his performance as Robin Oakapple, and the production, , as "funny and fast moving… theatre at its best." As a director he created innovative student productions of The Gondoliers, Patience, Pirates, Ruddigore and Pinafore for NYGASP and Lake George opera/Opera Saratoga. He has also choreographed productions of The Pirates of Penzance with Opera NJ and Die Fledermaus and Le Nozze di Figaro at the Copland School of Music. Along with studying for two summers at Centro Studi Italiani, in Italy, David was a scholarship recipient at the prestigious Manhattan School of Music where he received the Janet D. Schenck Award. David is a founding member of House of Murgatroyd Entertainment (H.O.M.E) and is the co-producer, and co-creator of H.O.M.E.'s critically-acclaimed production of "The House of Murgatroyd or Ruddygore Revisited".
CÁITLÍN BURKE, producer
Praised by the N.Y.Times for having "virtuoso flair", and the ability to create "three-dimensional characters", multi-talented artist, Cáitlín Burke's career has spanned the genres of Broadway, theatre, opera, and classical music. She most recently appeared, to critical acclaim, as The Mother Abbess at The Kennedy Center on the national tour of The Sound of Music, directed by three-time Tony award winner, Jack O'Brien. Internationally, she was the first American to tour with London's National Gilbert and Sullivan Opera Company, where she appeared at England's Royal Hall, as well as prestigious venues across the U.K., and has garnered rave reviews for her work in the U.K. at The International Gilbert & Sullivan Festival. She has frequently appeared as a principal artist at Lincoln Center, New York City Center, Symphony Space, the 92nd Street Y, The Times Center, The Kennedy Center, The Filene Center at Wolf Trap, The Ahmanson Theatre, North Shore Music Theatre, Meadow Brook Theatre, The National Arts Centre (Canada),
The Ed Mirvish Theatre (Toronto, Canada), The Boston Early Music Festival, Teatro Trevi (Trevi, Italy), Teatro Caio Melisso (Spoleto, Italy), Piazza de Municipio (Spoleto, Italy). Her stage work includes the regional premiere of Avenue Q (Best Supporting Actress Award), The King and I, South Pacific, Into the Woods, Bittersweet, Master Class, By Jeeves (Wilde Award nomination), M. Butterfly,The Miracle Worker, A Christmas Carol, The House of Murgatroyd, Amahl and the Night Visitors, Così Fan Tutte, Dido and Aeneas, and 10 seasons as a principal artist with The New York Gilbert and Sullivan players appearing in 11 Gilbert and Sullivan operettas.
Her concert work includes guest artist appearances with the U.K.'s National Festival Orchestra, the Columbus Symphony Orchestra, the Detroit Symphony Orchestra, the Rochester Symphony Orchestra, the Chattanooga Symphony, the Oakland Symphony, and the Detroit Chamber Winds. She is the recipient of the David Daniels artist award, the Elizabeth Gardner vocal award, Charlotte Ruppel vocal award, and was the first person to be honored with two Matilda Awards for Alumni Achievement in both Music and Theatre from Oakland University, where she received her bachelors degree before attending graduate school at Indiana University. Cáitlín is a founding member of House of Murgatroyd Entertainment (H.O.M.E) and is the co-producer, and co-creator of H.O.M.E.'s critically-acclaimed production of "The House of Murgatroyd or Ruddygore Revisited". www.CaitlinBurke.org
© 2018 by House of Murgatroyd Entertainment.
e-mail: SingChorusesInPublic@gmail.com


As the Muslims made attempts to understand God, they also tried to uncover the truth about human nature by conducting different researches and scientific investigations (Saud, 1994). For instance, the Muslims substituted the Roman number system existed in Spain for the Arabic number system that has been widely utilised in algebra, arithmetic and business since then. In addition, astronomy, medicine, biology and chemistry began to thrive in Spain after the Islamic invasion (Lewis, 1993). Among the most famous Spanish philosophers, writers, artists and scientists of the Muslim era are Al-Kwarizmi, Ibn Rushd, Ibn Zuhr, Al-Razi and Ibn Sina (Chejne, 1974). Ibn Sina's medical treatise Al-Qanun had been studied in many European educational establishments for about three hundred years and had been regarded as one of the best medical works .One of the greatest Muslim scholars of Spain was Abu Zakariyah al-Awwam Ishibili who created a procedure of grafting and gave names to more than five hundred plants (Ghazanfar, 2004). Pedro Alfonzo, a Spanish Muslim scholar who was interested in astronomy, claimed that his wish was to raise once more to life the knowledge of that science which is in such a deplorable state among those educated in the Latin manner (Hermes, 1977, p.72). Due to such an advanced stage of scientific development, many European scientists arrived to Spain to receive knowledge in various sciences and to interpret Latin texts. In regard to economics, the Muslims created the silk industry in Al-Andalus, gradually transforming Spain into one of the largest countries for silk production. The country was also engaged in the production of satin, cotton, pepper, furs, clocks, paper, maps and soaps. Further Spain contributed to the fine fabrics manufacturing in Europe. Agriculture was poorly developed in Spain because of a primordial irrigation system (White, 1970; Semple, 1971); but the Muslims substituted this old system for a new improved irrigation method that resulted in the prosperity of orchards and the increase of rice crops in such areas as Granada and the Valenican huerta.


Norton will not allow me to open PDF statements from my bank. This makes paperless banking impossible. Work-around tips appreciated.
What notification is Norton giving you concerning the PDF documents? What PDF program are you using?


Had candyfloss – We had been to a party and the Mum had arranged to have a candyfloss machine there. I tried to steer you away from it but the noise generated by your cheapnolvadexpct.com/generic-nolvadex/ classmates caught your attention. The sight of something blue and sticky that you could actually EAT (it wasn't Play-Doh) meant you were glued to the spot. Ten minutes later – and a lot of pushing and shoving in the queue – we were out. You were ecstatic and I resigned myself for a nightmare of an afternoon as your sugar levels rocketed off in to space.
Swam underwater – planned as well. It wasn't just because you were sinking.
Had your first class party – Following suit with the rest of your classmates I held a party for you. I only told you with an hour to go that you were having one. Your excitement was off the scale. Everyone was met with a squeal in some sort of high-pitched alien voice. You were most definitely the sweatiest, loudest and happiest one there. Two hours after the party ended I could still hear the noise of the children in my head. I made up food boxes and sweet cones for 30. I had wrapped pass the parcel, socialised with the parents and then tidied away. Note to self: Next year book a play barn and have them do everything. It's worth every penny!!!
Switched on the main light in your room without the need to use your step – Granted you still have to jump to reach it. Evidenced by the dirty hand marks on the wall.
Gymnastics medal – It wasn't for "The least likely gymnastic" but if the cap fits….
Had a slush drink – I refer you to the bullet point about the first taste of candyfloss. Different substance yet the same result.
Went bowling – You came last so the less said about that the better. On the plus side you have plenty of time to practice before you suggest it to someone as a date.


text:
Eventi in diretta
Produzioni originali
Giochi olimpici
Giochi e Medaglie
Atene 2004
Weightlifting Light-Heavyweight (≤85 kilograms)
Sydney 2000 2000
Atlanta 1996 1996
Weightlifting Light-Heavyweight (≤82½ kilograms)
Pyrros DIMAS
173 cm / 5'8''
84 kg / 184 libbre
13 ott 1971 Himarë, Albania
Numero di medaglie
4 Medaglie Olimpiche
4 Giochi Olimpici
Pyrros DIMAS: biografia
Born in Himare, Albania as Pirro Dhima, Dimas emigrated to Greece in 1991, and has since become one of the greatest lifters ever. He has won four Olympic medals, including three consecutive gold medals from 1992-2000, and equaling the feat of Norb Schemansky with medals at four consecutive Olympics. At the World Championships he won four medals, with golds in 1993, 1995, and 1998. He won one European Championship in 1995. As a light-heavyweight, he has set 11 world records. His brother, Odysseas Dimas, is also a national champion weightlifter.
TM © Olympic Channel Services S.L. 2021 – Tutti i diritti riservati


One of the toughest things to do for lawn care involves getting your lawn ready and treated correctly during a drought. This is because a drought can be a time when your lawn isn't going to get all of the cold spring water that it needs in order for it to survive. You'll need to ensure that your lawn will be treated properly if you want it to survive in this tough condition when you may not be able to find enough water ready.
You may use your dish wash pub for cleaning carpet. Mix together 1/4 teaspoon of dishwashing soap and one quart of tampines hub swimming pool this will go a long way. Use a small amount of this option and using your fingers, press into stain. Blot excess liquid. Repeat until no stain appears on white paper towels.
Costumes and props. First, it's not easy to bring animals into life. They operate well to wear costumes and make ups to perfectly perform their roles as animals. Additionally, they're actually using props that made them look like are real one.
No matter how much control one has over another, it will never bring inner peace. Anyone that has not found inner peace should look to their activities to find the reason. Remember – there are very, very few situations where – I was a victim and it was not my fault, or someone made me do it – actually holds true. Excuses for actions will solve nothing and those individuals will remain in their self induced quagmire rather than finding the path to the Light.
Another way to work exercise into your life in ways which are hardly noticeable is to find a hobby that needs physical activity. Going for a hike on a bright autumn day will feel like a break from the norm. You'll be so busy relaxing; you will not even realize you are getting exercise. You can even work in exercise by taking up pleasure past times such as rollerblading, rock climbing, surfing, swimming, or tennis. If you want to combine social fun with exercise, consider joining a local group.
It's different cottages with a slightly different feel for tourists and guests to choose from. Rustic family cottage, country cottages and one suite spread in the 7 acres of the place. All of these are adorned with all the amenities in addition to things of beauty and magnificence.
Purchasing a horse lover is rather simple when you open your eyes to see all of the possibilities out there. Whether you would like to spend a little or a lot on a horse present, there are a lot of options. So the next time you have a horse lover on your gift list, you'll know just what type of gift to go for.


text:
Last-minute save lifts Qatar past Japan
H.H. Sheikh Abdullah bin Zayed, FM of Cyprus review advancing cooperation
UAE President confers Zayed the Second Medal to US Ambassador
Guidi (ITA) and de Jesus Soares (BRA) take first Beach Games gold
October 14, 2019 businessarabia.qa
DOHA, Marcello Guidi (ITA) and Brazil's Ana de Jesus Soares wrote themselves into the history books this morning at Katara Beach in the Open Water 5 Km swim by not only winning the first gold medals awarded at the World Beach Games Qatar 2019, but the first in the history of the event.
Despite an earlier-than-usual start time of 6 a.m., the water temperature still hovered over 30 degrees Celsius at the start of the race, and choppy surf nearly toppled some athletes off the pontoon before the horn.
For the 5 Km distance, competitors navigated four laps of a 1.25-kilometre course.
In the men's race, Germany's Soeren Meissner swam to the head of the lead pack of about 10 swimmers after one and-a-half laps and led for the majority of the race. Guidi, who had not won an international event prior to this, sprinted ahead with only 40 metres to go to take gold in a time of 55:25. As Meissner faltered in the last few metres, Denis Adeev (RUS) was also able to pass the German for silver in 55:26. Meissner, part of the powerhouse German world champion squad in the team event, rounded out the medallists in 55:28.
"It was really hard in the end, and two guys passed me," Meissner admitted after he emerged from the water. "I was first at the last buoy, but it was so hard for me at the end."
Heavy favourite Kristof Rasoovszky, who won the 2019 World Championships in the 5k by an astonishing 10 seconds, placed 17th.
On the women's side, de Jesus Soares, the reigning World champion in the 5k and Pan American champion in the 10k, placed herself in the lead early on and never relinquished it, winning gold in a time of 59:51.
"When you race, you know when you have space," the Brazilian said. "You feel the touch of others at your feet. Today, I didn't feel them touching my feet, so I knew I had a little more space for the finish."
Although the Brazilian felt metres ahead of her competition, China's Yawen Hou hit the board a second later, with Leonie Beck (GER) in third in 59:53 to add to her bronze in the same distance from the world championships earlier this year.
Local swimmers, Abdurrahman Mohammed Hisham and Nada Mohammed Wafa made impressive participation in the swimming event.
Source: Qatar Olympic Committee
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text:
The PJ Tatler
Media Shield Bill Puts Into Writing What Holder Vowed After AP Scandal
By Bridget Johnson Jul 17, 2013 3:20 PM ET
A bipartisan group of senators led by Lindsey Graham (R-S.C.) and Chuck Schumer (D-N.Y.) are attempting to write into law vows made by the Justice Department after the AP phone records scandal.
The media shield legislation originally offered, the Free Flow of Information Act of 2013, "protects journalists and their employers from having to reveal information, including source identity, that a reporter obtains under a promise of confidentiality and in the course of carrying out newsgathering functions," with exceptions for classified leak cases or when the information would prevent or mitigate terrorism, death, kidnapping, and bodily harm. There's also an exception for journalists who obtain their information "through observation or perpetration of a criminal act" other than leaking.
The new language to codify into law and expand the DOJ's new media guidelines will be added in the amendment process.
"A free press remains essential to our democracy," said Graham. "The media shield law tries to bring balance between those who report the news all the while protecting our national security. I believe the legislation, which will continue to be improved as the process moves forward, will ultimately strike the appropriate balance of protecting journalists and protecting our national security."
The amendment will limit to just once the number of times the Justice Department can ask the a court for an extension on the amount of time it can take to notify a journalist that his or her records have been sought. Under the legislation, the DOJ would have a maximum of 90 days before it has to tell news outlets they're being snooped on.
"The DOJ guidelines were a promising start, but this bill ensures that they can't be changed on a whim, and goes beyond the guidelines to ensure that we balance our national security needs against the public's right to the free flow of information," said Schumer. "These changes make the bill stronger and should provide added momentum to get it passed."
Prosecutors would bear the burden of convincing a judge that the information at issue would "prevent or mitigate an act of terrorism or harm to national security."
Sens. Richard Blumenthal (D-Conn.), Roy Blunt (R-Mo.), Johnny Isakson (R-Ga.), Amy Klobuchar (D-Minn.), and Jon Tester (D-Mont.) signed on to the Schumer-Graham effort.
"I supported similar bills in the House in 2007 and 2009, and I think this bipartisan bill is an improvement on that legislation. I'm proud to be part of this effort, and I will continue my commitment to protecting Americans' First Amendment rights," said Blunt.


text:
Anne de Bourbon (1380 - septembre 1408) est la fille de Jean Ier de Bourbon-La Marche et de Catherine de Vendôme. Elle est membre de la maison de Bourbon-La Marche.

Famille
Anne est l'un des sept enfants de Jean Ier de Bourbon-La Marche et de Catherine de Vendôme. Ses frères et sœurs sont Jacques II de Bourbon-La Marche, Louis Ier de Bourbon-Vendôme, Jean de Bourbon-Carency et la reine de Chypre Charlotte de Bourbon. Par sa sœur, Anne est la tante de Jean II de Chypre et d'Anne de Lusignan, duchesse de Savoie. Elle a également un demi-frère illégitime né de son père.

Les grands-parents paternels d'Anne sont Jacques Ier  de Bourbon-La Marche et Jeanne de Châtillon. Ses grands-parents maternels sont Jean VI de Vendôme et Jeanne de Ponthieu.

Premier mariage
En 1390, Anne devient la deuxième épouse du comte de Montpensier Jean de Berry, petit-fils de Jean II de France. Sa première épouse Catherine de France étant décédée à l'âge de 10 ans, Jean a besoin d'un héritier. Cependant, comme son premier mariage, cette union ne produit aucun enfant survivant. Jean meurt en 1397, laissant Anne disponible pour un second mariage.

Second mariage
Le 1er octobre 1402 à Paris, Anne se remarie avec Louis VII de Bavière, frère de la reine Isabeau de Bavière. Il succède à son père comme duc de Bavière en 1413, cinq ans après la mort d'Anne. Ils ont un fils :

 Louis VIII de Bavière (1er septembre 1403 - 7 avril 1445)

Anne meurt en septembre 1408 et est inhumée dans l'église aujourd'hui démolie du Couvent des Jacobins à Paris. Louis se remarie avec Catherine d'Alençon en 1413.

Ascendance

Personnalité française du XVe siècle
Personnalité française du XIVe siècle
Maison de Bourbon-La Marche
Décès en 1408
Naissance en 1380
Comtesse de Montpensier

redpajama_set_name: RedPajamaWikipedia


text:
Q: Given a graph with distinct edge weights and a not-minimum ST, there always exist another ST of lesser total weight that differs only by one edge I have to show that, if all the edge weights of a graph are distinct, given a spanning tree $T$ that is not a MST, there always exist a spanning tree $T'$ of lesser total weight, s.t. $T'$ differs from $T$ only by one edge.
I started reasoning from this question, but it's not helpful for my case and I cannot go over.

A: Actually that question (in particular this answer) is helpful.
A proof using cycle property:
Let $G=(V,E)$ be the original graph. Let the set of edges $T \subseteq E$ be a spanning tree on $G$ that is not minimum.
Now, there will exist an edge $e$ which belongs to the MST and not to $T$.
Adding $e$ it to $T$ creates a cycle. By cycle property, the most expensive edge of this cycle (call it $e'$) does not belong to the MST, so it must belong to $T$.
Removing $e'$ we break the cycle and we obtain a new subgraph $T'$ with lesser total weight than $T$. Furthermore, $T'$ is a spanning tree because:

*

*It doesn't have cycles: we broke the cycle removing $e'$.

*It is connected: creating and breaking a cycle cannot affect connectivity.

*It covers all the vertices of $G$: the two vertices of the removed edge $e'$ are still covered by the adjacent edges of $e'$.

So there must exist a spanning tree of lesser total weight, s.t. it differs from $T$ only by one edge.

A: Consider a spanning tree $E$ and label its edges $e_1$, $\ldots$,$e_n$. Consider now a spanning tree $F$. Then there exists a labeling of the edges of $F$ $\  $ $f_1$, $\ldots$, $f_n$ so that the following are still spanning trees (use an exchange lemma like for two bases of a vector space):
$$(e_1, e_2, \ldots, e_{n-1},e_n) \\
  (e_1, e_2, \ldots, e_{n-1},f_n)\\
  (e_1, e_2, \ldots, f_{n-1}, f_n)\\
   \ldots \\
  (e_1, f_2, \ldots, f_{n-1}, f_n)\\
  (f_1, f_2, \ldots, f_{n-1}, f_n)$$
Assume now that $E$ is obtained using the greedy algorithm:
$e_1$ is of minimal weight, $e_2$ is of minimal weight so that $e_1$, $e_2$ form no cycles, $e_3$ is of minimal weight so that
$e_1$, $e_2$, $e_3$ form no cycles, and so on, up to $e_n$. From the above we conclude that $w(e_i) \le w(f_i)$ for all $i$.
Since $F$ is arbitrary we conclude that $E$ is a minimal tree.
Now assume that $F$ itself is not a minimal  tree. Then for some $i$ we have a strict inequality $w(e_i) < w(f_i)$.
 Let $i$ the smallest index for which this happens. Let's assume now that all the edges have different weights. Then
we have $e_1= f_1$, $\ldots$,$e_{i-1} =f_{i-1}$. Hence the tree $(e_1, \ldots, e_{i-1}, f_{i}, \ldots, f_n)$ is $F$ and
the tree $(e_1, \ldots, e_{i-1}, e_i, f_{i+1}, \ldots, f_n)$ is obtained from it by exchanging the edge $e_i$ with an edge of
larger weight $f_i$.

A: This is true even if not all the edge weights are distinct.
Define
$$ w'(e) = \begin{cases} 2 \cdot w(e) &\text{ if } e \text{ belongs to } T \\ 2 \cdot w(e) + 1 & \text{otherwise}\end{cases} $$
then sort all the edges according to $w'$ (rather than $w$). Observe that it produces the same ordering as sorting according to $w$ only that it prioritizes edges of $T$ if possible. Now run the Kruskal's algorithm using that new ordering and denote by $e$ the first edge not in $T$ that was chosen by the algorithm.
Let $e'$ be the heaviest edge on the cycle created by $e$ in $T \cup \{e\}$. Observe that $e$ does not create a cycle with edges of strictly smaller $w'$, otherwise it would not be chosen by the algorithm. Thus $w'(e) \leq w'(e')$, and so $w(e) < w'(e')$, because $e$ is not in $T$ while $e'$ is. Therefore we can set $T' = T \setminus \{e'\} \cup \{e\}$.
I hope this helps $\ddot\smile$

redpajama_set_name: RedPajamaStackExchange


The turtlebacks in the decorative band of this 18″ Turtleback shade are narrow and wide, accentuating the horizontal look of the piece. This shade is made from a rippled glass in yellow green/spring green that has hints of light blue throughout. The rippled surface of the glass faces the interior of the shade, so when unlit the shade appears smooth and comes to life when illuminated. Commissioned by a Texas client in 2011, this 18″ Turtleback shade is shown on the Decorated Library base.


In this issue, we take a closer look at the utilization of "multiple criteria decision analysis" (MCDA) in health technology appraisals, newer therapies for Cystic Fibrosis, and the regulatory pathways and complexity of health technology assessment (HTA) evidentiary hurdles for new diabetes drugs, devices, and combination technologies.
We examine wearable technology and big data, valuing CAR-T therapies, and a look at Catalonia and the region's autonomous healthcare market.
We examine the world's second largest pharmaceuticals market as Japan shifts from a traditional reimbursement assessment. We look at new therapies for Tardive Dyskinesea. We also review Taiwan's Center for Drug Evaluation on its 10 year anniversary.
We examine oncology appraisal differences between NICE and SMC, market access for cell and gene therapies, and managed entry agreements.
We examine medical nutrition reimbursement, severe asthma therapies, and brazil's healthcare market.
We take a look at patient input into HTA decisions in 4 countries, examining new therapies for Duchenne Muscular Dystrophy, and understanding the Colombian universal healthcare model.
We examine the process to appeal unfavorable NICE decisions, provide insights on immunotherapy coverage and reimbursement, and take a deeper look at global value dossiers.
We examine indication-specific pricing in Europe and in the US, approved therapies for multiple myeloma, and take a closer look at Portugal's HTA body, SiNATS.
We examine rapid access in the US, UK, and France, targeted therapies for psoriasis and psoriatic arthritis, and explore Singapore's highly efficient healthcare system.


Size: 74 in H x 26 in W x 20 in D.
Finish shown: Antique Grey (white with grey wash) and Yellow White (white with yellow wash).
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It's a new year and that means a new you! Make 2019 the year to take a few risks when it comes to your style as well as your travel choices. For this edition of New Year New You, we've provided you with a selection of the best places to travel in 2019 according to Travel + Leisure along with outfits for each location. Some of these locations might be new to you, and that's ok! Here at Front Door Fashion, our resolution is to get you wherever you're going in style and to push you a little outside your comfort zone. From beaches to the mountains, FDF has you covered with looks for every destination!
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Resolving to travel more falls under the category of FUN when it comes to New Year's Resolutions. Make 2018 the year to check a few dream locations off your bucket list! Here at Front Door Fashion, our resolution is to get you wherever your are going in style. For this edition of New Year New You, we've provided you with a selection of the best places to travel in 2018 according to Travel + Leisure, along with outfits for each location. Spend less time shopping and more time experiencing with these travel-friendly outfits to make your trip even more memorable. From beaches to European backstreets, FDF has you covered with looks for every destination!


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text:
For other uses of the word mumps, see Mumps (disambiguation).
Epidemic parotitis
Child with mumps
Parotitis and non-specific symptoms such as fever, headache, malaise, muscle pain, and loss of appetite
Deafness, inflammatory conditions such as orchitis, oophoritis, and pancreatitis, and rarely sterility
Usual onset
7–25 days after exposure
Usually less than two weeks
Mumps virus
Exposure to someone with mumps
Diagnostic method
Antibody testing, viral cultures, and reverse transcription polymerase chain reaction
Pain medication, intravenous immunoglobulin
Usually excellent; case fatality rate of 1.6–3.8 people per 10,000
Most common in childhood and in countries that do not vaccinate
Mumps is a viral disease caused by the mumps virus. Initial symptoms are non-specific and include fever, headache, malaise, muscle pain, and loss of appetite. These symptoms are usually followed by painful swelling of the parotid glands, called parotitis, which is the most common symptom of infection. Symptoms typically occur 16 to 18 days after exposure to the virus and resolve within two weeks. About one third of infections are asymptomatic.
Complications include deafness and a wide range of inflammatory conditions, of which inflammation of the testes, breasts, ovaries, pancreas, meninges, and brain are the most common. Testicular inflammation may result in reduced fertility and, rarely, sterility.
Humans are the only natural host of the mumps virus, an RNA virus in the family Paramyxoviridae. The virus is primarily transmitted by respiratory secretions such as droplets and saliva, as well as via direct contact with an infected person. Mumps is highly contagious and spreads easily in densely populated settings. Transmission can occur from one week before the onset of symptoms to eight days after. During infection, the virus first infects the upper respiratory tract. From there, it spreads to the salivary glands and lymph nodes. Infection of the lymph nodes leads to presence of the virus in blood, which spreads the virus throughout the body. Mumps infection is usually self-limiting, coming to an end as the immune system clears the infection.
In places where mumps is common, it can be diagnosed based on clinical presentation. In places where mumps is less common, however, laboratory diagnosis using antibody testing, viral cultures, or real-time reverse transcription polymerase chain reaction may be needed. There is no specific treatment for mumps, so treatment is supportive in nature and includes bed rest and pain relief. Prognosis is usually excellent with a full recovery as death and long-term complications are rare. Infection can be prevented with vaccination, either via an individual mumps vaccine or through combination vaccines such as the MMR vaccine, which also protects against measles and rubella. The spread of the disease can also be prevented by isolating infected individuals.
Mumps historically has been a highly prevalent disease, commonly occurring in outbreaks in densely crowded spaces. In the absence of vaccination, infection normally occurs in childhood, most frequently at the ages of 5–9. Symptoms and complications are more common in males and more severe in adolescents and adults. Infection is most common in winter and spring in temperate climates, whereas no seasonality is observed in tropical regions. Written accounts of mumps have existed since ancient times, and the cause of mumps, the mumps virus, was discovered in 1934. By the 1970s, vaccines had been created to protect against infection, and countries that have adopted mumps vaccination have seen a near-elimination of the disease. In the 21st century, however, there has been a resurgence in the number of cases in many countries that vaccinate, primarily among adolescents and young adults, due to multiple factors such as waning vaccine immunity and opposition to vaccination.
1 Signs and symptoms
1.1 Common symptoms
1.2 Complications
2 Cause
4 Pathogenesis
5 Immune response
8 Prognosis
10 Epidemiology
11.1 Resurgence
11.2 Etymology
Signs and symptoms[edit]
Common symptoms[edit]
The incubation period, the time between the start of infection and when symptoms begin to show, is about 7–25 days,[1][2] averaging 16–18 days.[3] 20-40%[4] of infections are asymptomatic or are restricted to mild respiratory symptoms, sometimes with a fever.[5][6] Over the course of the disease, three distinct phases are recognized: prodromal, early acute, and established acute. The prodromal phase typically has non-specific, mild symptoms such as a low-grade fever, headache, malaise, muscle pain, loss of appetite, and sore throat.[5][7][8] In the early acute phase, as the mumps virus spreads throughout the body, systemic symptoms emerge. Most commonly, parotitis occurs during this time period. During the established acute phase, orchitis, meningitis, and encephalitis may occur, and these conditions are responsible for the bulk of mumps morbidity.[5]
The parotid glands are salivary glands situated on the sides of the mouth in front of the ears. Inflammation of them, called parotitis, is the most common mumps symptom and occurs in about 90%[9] of symptomatic cases and 60-70% of total infections.[10] During mumps parotitis, usually both the left and right parotid glands experience painful swelling,[10] with unilateral swelling in a small percentage of cases.[6] Parotitis occurs 2–3 weeks after exposure to the virus, within 2 days of developing symptoms, and usually lasts for 2–3 days, but it may last as long as a week or longer.[5][7]
In 90% of parotitis cases, swelling on one side is delayed rather than both sides swelling in unison.[10] The parotid duct, which is the opening that provides saliva from the parotid glands to the mouth, may become red, swollen, and filled with fluid. Parotitis is usually preceded by local tenderness and occasionally earache.[2][11] Other salivary glands, namely the submaxillary, submandibular, and sublingual glands, may also swell. Inflammation of these glands is rarely the only symptom.[5]
Complications[edit]
Outside of the salivary glands, inflammation of the testes, called orchitis, is the most common symptom infection. Pain, swelling, and warmness of a testis appear usually 1–2 weeks[12] after the onset of parotitis but can occur up to 6 weeks later. During mumps orchitis, the scrotum is tender and inflamed. It occurs in 10-40% of pubertal and post-pubertal males who contract mumps. Usually, mumps orchitis affects only one testis but in 10–30%[12] of cases both are affected. Mumps orchitis is accompanied by inflammation of the epididymis, called epididymitis, about 85% of the time, typically occurring before orchitis. The onsent of mumps orchitis is associated with a high-grade fever, vomiting, headache, and malaise.[5][10] In prepubertal males, orchitis is rare as symptoms are usually restricted to parotitis.[10]
A variety of other inflammatory conditions may also occur as a result of mumps virus infection, including:[5]
Mastitis, inflammation of the breasts, in up to about 30% of post-pubertal women[13]
Oophoritis, inflammation of an ovary, in 5-10% of post-pubertal women, which usually presents as pelvic pain
Aseptic meningitis, inflammation of the meninges, in 5-10% of cases[14] and 4-6% of those with parotitis, typically occurring 4-10 days after the onset of symptoms. Mumps meningitis can also occur up to one week before parotitis as well as in the absence of parotitis. It is commonly accompanied by fever, headache, vomiting, and neck stiffness.[15]
Pancreatitis, inflammation of the pancreas, in about 4% of cases, which causes severe pain and tenderness in the upper abdomen below the ribs
Encephalitis, inflammation of the brain, in less than 0.5% of cases.[14] People who experience mumps encephalitis typically experience a fever, altered consciousness, seizures, and weakness. Like meningitis, mumps encephalitis can occur in the absence of parotitis.[15]
Meningoencephalitis, inflammation of the brain and its surrounding membranes. Mumps meningoencephalitis is commonly accompanied by fever 97% of the time, vomiting 94% of the time, and headache 88.8% of the time.[16]
Nephritis, inflammation of the kidneys, which is rare because kidney involvement in mumps is usually benign but leads to presence of the virus in urine
Inflammation of the joints (arthritis), which may affect at least five joints (polyarthritis),[17] multiple nerves in the peripheral nervous system (polyneuritis), pneumonia,[2] gallblader without gallstones (acalculous cholecystitis), cornea and uveal tract (keratouveitis), thyroids (thyroiditis), liver (hepatitis), retina (retinitis), and corneal endothelium (corneal endothelitis), all of which are rare[5][13]
Recurrent sialadenitis, inflammation of the salivary glands, which is frequent[2]
A relatively common complication is deafness, which occurs in about 4% of cases.[9] Mumps deafness is often accompanied by vestibular symptoms such as vertigo and repetitive, uncontrolled eye movements. Based on electrocardiographic abnormalities in the infected, MuV also likely infects cardiac tissue, but this is usually asymptomatic. Rarely, myocarditis and pericarditis can occur. Fluid buildup in the brain, called hydrocephalus, has also been observed.[5][15] In the first trimester of pregnancy, mumps may increase the risk of miscarriage. Otherwise, mumps is not associated with birth defects.[11][13]
Other rare complications of infection include: paralysis, seizures, cranial nerve palsies, cerebellar ataxia, transverse myelitis, ascending polyradiculitis, a polio-like disease, arthropathy, autoimmune hemolytic anemia,[5] idiopathic thrombocytopenic purpura, Guillain–Barré syndrome, post-infectious encephalitis[13] encephalomyelitis,[17] and hemophagocytic syndrome.[10] At least one complication occurs in combination with the standard mumps symptoms in up to 42% of cases.[10] Mumps has also been connected to the onset of type 1 diabetes, and, relatedly, the mumps virus is able to infect and replicate in insulin-producing beta cells.[18] Among children, seizures occur in about 20-30% of cases involving the central nervous system.[11]
Cause[edit]
Mumps is caused by the mumps virus (MuV), scientific name Mumps orthorubulavirus, which belongs to the Orthorubulavirus genus in the Paramyxoviridae family of viruses.[19] Humans are the only natural host of the mumps virus. MuV's genome is made of RNA and contains seven genes that encode nine proteins. In MuV particles, the genome is encased by a helical capsid. The capsid is surrounded by a viral envelope that has spikes protruding from its surface. MuV particles are pleomorphic in shape and range from 100 to 600 nanometers in diameter.[5][20][21]
The replication cycle of MuV begins when the spikes on its surface bond to a cell, which then causes the envelope to fuse with the host cell's cell membrane, releasing the capsid into the host cell's cytoplasm.[5][22][23] Upon entry, the viral RNA-dependent RNA polymerase (RdRp) transcribes messenger RNA (mRNA) from the genome, which is then translated by the host cell's ribosomes to synthesize viral proteins. RdRp then begins replicating the viral genome to produce progeny.[5][23] Viral spike proteins fuse into the host cell's membrane, and new virions are formed at the sites beneath the spikes.[5][22][23] MuV then utilizes host cell proteins to leave the host cell by budding from its surface, using the host cell's membrane as the viral envelope.[22]
Twelve genotypes of MuV are recognized, named genotypes A to N, excluding E and M. These genotypes vary in frequency from region to region. For example, genotypes C, D, H, and J are more common in the western hemisphere, whereas genotypes F, G, and I are more common in Asia, although genotype G is considered to be a global genotype. Genotypes A and B have not been observed in the wild since the 1990s. MuV has just one serotype, so antibodies to one genotype are functional against all genotypes.[9] MuV is a relatively stable virus and is unlikely to experience antigenic shifting that may cause new strains to emerge.[2]
Transmission[edit]
The mumps virus is mainly transmitted by inhalation or oral contact with respiratory droplets or secretions. In experiments, mumps could develop after inoculation either via the mouth or the nose. Respiratory transmission is also supported by the presence of MuV in cases of respiratory illness without parotitis, detection in nasal samples, and transmission between people in close contact.[5] MuV is excreted in saliva from approximately one week before to eight days after the onset of symptoms,[1] peaking at the onset of parotitis,[4] though it has also been identified in the saliva of asymptomatic individuals.[5]
Mother-to-child transmission has been observed in various forms. In non-human primates, placental transmission has been observed, which is supported by isolation of MuV from spontaneous and planned aborted fetuses during maternal mumps. MuV has also been isolated from newborns whose mother was infected. While MuV has been detected in breast milk, it is unclear if the virus can be transmitted through it.[5] Other manners of transmission include direct contact with infected droplets or saliva, fomites contaminated by saliva, and possibly urine.[4][10][12] Most transmissions likely occur before the development of symptoms and up to five days after such time.[4]
In susceptible populations, a single case can cause up to 12 new cases. The time period when a person is contagious lasts from two days before the onset of symptoms to nine days after symptoms have ceased. Asymptomatic carriers of the mump virus can also transmit the virus.[10] These factors are thought to be reasons why controlling the spread of mumps is difficult.[5] Furthermore, reinfection can occur after a natural infection or vaccination,[9] indicating that lifelong immunity is not guaranteed after infection.[14] Vaccinated individuals who are infected appear to be less contagious than the unvaccinated.[4]
The average number of new cases generated from a single case in a susceptible population, called the basic reproduction number, is 4–7. Given this, it is estimated that a vaccination rate between 79–100% is needed to achieve herd immunity. Outbreaks continue to occur in places that have vaccination rates exceeding 90%, however, suggesting that other factors may influence disease transmission. Outbreaks that have occurred in these vaccinated communities typically occur in highly crowded areas such as school and military dormitories.[24]
Pathogenesis[edit]
Many aspects of the pathogenesis of mumps are poorly understood and are primarily inferred based on observations from the clinical features of the disease and experimental infections in laboratory animals. These animal studies may be unreliable for various reasons, including unnatural methods of inoculation.[5] Following exposure, the virus infects epithelial cells in the upper respiratory tract that express sialic acid receptors on their surface. After initial infection, the virus spreads to the parotid glands, causing the signature parotitis.[15] It is thought that shortly after infection the virus spreads to lymph nodes, in particular T-cells, which results in the presence of viruses in the blood, called viremia.[1][5] Viremia lasts for 7–10 days, during which MuV spreads throughout the body.[10]
In mumps orchitis, infection leads to: parenchymal edema; congestion, or separation, of the seminiferous tubules; and perivascular infilitration by lymphocytes. The tunica albuginea forms a barrier against edema, causing an increase in intratesticular pressure that causes necrosis of the seminiferous tubules. The seminiferous tubules also experience hyalinization, i.e. degeneration into a translucent glass-like substance, which can cause fibrosis and atrophy of the testes.[10][12]
In up to half of cases, MuV infiltrates the central nervous system (CNS), where it may cause meningitis, encephalitis, or hydrocephalus. Mumps is rarely fatal, so few post-mortem analyses have been done to analyze CNS involvement. Of these, fluid buildup, congestion, and hemorrhaging in the brain, white blood cell infilitration in the perivascular spaces in the brain, reactive changes to glial cells and damage to the myelin sheaths surrounding neurons were observed. Neurons appear to be relatively unaffected.[5]
In laboratory tests on rodents, MuV appears to enter the CNS first through cerebrospinal fluid (CSF), then spreading to the ventricular system. There, MuV replicates in ependymal cells that line the ventricles, which allows the virus to enter the brain parenchyma. This often leads to MuV infecting pyramidal cells in the cerebral cortex and hippocampus. Infected ependymal cells become inflamed, lose their cilia, and collapse into CSF, which may be the cause of the narrowing of the cerebral aqueduct thought to cause mumps hydrocephalus.[5]
In humans, mumps hydrocephalus may be due to obstruction of the cerebral aqueduct with dilatation of the lateral and third ventricles, obstruction of the interventricular foramina, or obstruction of the median and lateral apertures. Ependymal cells have been isolated from CSF of mumps patients, suggesting that animals and humans share hydrocephalus pathogenesis. Hydrocephalus has also been observed in the absence of canal obstruction, however, indicating that obstruction may be a result of external compression by edematous tissue and not related to hydrocephalus.[5]
Deafness from mumps may be caused by MuV infection in CSF, which has contact with the perilymph of the inner ear, possibly leading to infection of the cochlea, or it may occur as a result of inner ear infection via viremia that leads to inflammation in the endolymph. Hearing loss may also be caused indirectly by the immune response. In animal studies, MuV has been isolated from the vestibular ganglion, which may explain vestibular symptoms such as vertigo that often co-occur with deafness.[5]
Immune response[edit]
Even though MuV has just one serotype, significant variation in the quantity of genotype-specific sera needed to neutralize different genotypes in vitro has been observed.[14][25] Neutralizing antibodies in the salivary glands may be important in restricting MuV replication and transmission via saliva, as the level of viral secretion in saliva inversely correlates to the quantity of MuV-specific IgA produced.[1] The neutralizing ability of salivary IgA appears to be greater than serum IgG and IgM.[4]
It has been proposed that symptomatic infections in the vaccinated may be because memory T lymphocytes generated as a result of vaccination may be necessary but insufficient for protection. The immune system in general appears to have a relatively weak response to the mumps virus, indicated by various measures: antibody production appears to be predominately directed toward non-neutralizing viral proteins, and there may possibly be a low quantity of MuV-specific memory B lymphocytes. The amount of antibodies needed to confer immunity is unknown.[14]
Diagnosis[edit]
In places where mumps is widespread, diagnosis can be made based on development of parotitis and history of exposure to someone with mumps. In places where mumps is less common, because parotitis has other causes, laboratory diagnosis may be needed to verify mumps infection.[9] A differential diagnosis may be used to compare symptoms to other diseases, including allergic reaction, mastoiditis, measles, and pediatric HIV infection and rubella.[2] MuV can be isolated from saliva, blood, the nasopharynx, salivary ducts,[7] and seminal fluid within one week of the onset of symptoms,[10] as well as from cell cultures.[9] In meningitis cases, MuV can be isolated from CSF.[15] In CNS cases, a lumbar puncture may be used to rule out other potential causes,[13] which shows normal opening pressure,[11] more than 10 leukocytes per cubic millimeter, elevated lymphocyte count in CSF, polymorphonuclear leukocytes up to 25% of the time, often a mildly elevated protein level, and a slightly reduced glucose ratio up to 30% of the time.[15]
Mumps-specific IgM antibodies in serum or oral fluid specimens can be used to identify mumps. IgM quantities peak up to 8 days after the onset of symptoms,[9] and IgM can be measured by enzyme-linked immunosorbent assays (ELISA) 7–10 days after the onset of symptoms. Sensitivity to IgM testing is variable, ranging from as low as 24–51%[10] to 75% in the first week and 100% thereafter.[11] Throughout infection, IgM titres increase four-fold between the acute phase and recovery.[10] False negatives can occur in people previously infected or vaccinated, in which case a rise is serum IgG may be more useful for diagnosis. False positives can occur after infection of parainfluenza viruses 1 and 3 and Newcastle disease virus as well as recently after mumps vaccination.[7][17]
Antibody titers can also be measured with complement fixation tests, hemagglutination assays, and neutralization tests.[15] In vaccinated people, antibody-based diagnosis can be difficult since IgM often times cannot be detected in acute phase serum samples. In these instances, it is easier to identify MuV RNA from oral fluid, a throat swab, or urine.[9] In meningitis cases, MuV-specific IgM can be found in CSF in half of cases, and IgG in a 30–90%, sometimes lasting for more than a year with increased white blood cell count. These findings are not associated with increased risk of long-term complications.[11][17] Most parotitis cases have elevated white blood cell count in CSF.[15]
Real-time reverse transcription polymerase chain reaction (rRT-PCR) can be used to detect MuV RNA from the first day that symptoms appear, declining over the next 8–10 days.[9] rRT-PCR of saliva is typically positive from 2–3 days before parotitis develops to 4–5 days after and has a sensitivity of about 70%.[17] Since MuV replicates in kidneys, viral culture and RNA detection in urine can be used for diagnosis up to two weeks after symptoms begin,[11] though rRT-PCR used to identify the virus in urine has a very low sensitivity compared to virus cultures at below 30%.[17] In meningoencephalitis cases, a nested RT-PCR is able to detect MuV RNA in CSF up to two years after infection.[11]
In sialadenitis cases, imaging shows enlargement of the salivary glands, fat stranding, and thickening of the superficial cervical fascia and platysma muscles, which are situated on the front side of the neck. If parotitis only occurs one side, then detection of mumps-specific IgM antibodies, IgG titer, or PCR is required for diagnosis.[6] In cases of pancreatitis, there may be elevated levels of lipase or amylase, an enzyme found in saliva and the pancreas.[11][15][26][27]
Mumps orchitis is usually diagnosed by white blood cell count, with normal differential white blood cell counts. A complete blood count can show above or below average white blood cell count and an elevated C-reactive protein level. Urine analysis can exclude bacterial infections. If orchitis is present with normal urine analysis, negative urethral cultures, and negative midstream urine, then that can indicate mumps orchitis. Ultrasounds typically show diffuse hyper-vascularity, increased volume of the testes and epididymis, lower than usual ability to return ultrasound signals, swelling of the epididymis, and formation of hydroceles. Echo color doppler ultrasound is more effective at detecting orchitis than ultrasound alone.[10]
Treatment[edit]
Mumps is usually self-limiting, and no specific antiviral treatments exist for it, so treatment is aimed at alleviating symptoms and preventing complications. Non-medicinal ways to manage the disease include bed rest, using ice or heat packs on the neck and scrotum, consuming more fluids, eating soft food, and gargling with warm salt water.[8][10] Anti-fever medications may be used during the febrile period,[13] excluding aspirin when given to children, which may cause Reye syndrome.[8] Analgesics may also be provided to control pain from mumps inflammatory conditions.[13] For seizures, anticonvulsants may be used. In severe neurological cases, ventilators may be used to support breathing.[11]
Intramuscular mumps immunoglobulin may be of benefit when administered early in some cases, but it has not shown benefit in outbreaks. Although not recommended, intravenous immunoglobulin therapy may reduce the rates of some complications.[10] Antibiotics may be used as a precaution in cases in which bacterial infection cannot be ruled out as well as to prevent secondary bacterial infection.[10][12] Autoimmune-based disorders connected to mumps are treatable with intravenous immunoglobulin.[13]
Various types of treatment for mumps orchitis have been be used, but no specific treatment is recommended due to each method's limitations. These measures are primarily based around relieving testicular pain and reducing intratesticular pressure to reduce the likelihood of testicular atrophy.[10][12] Interferon-α2α interferes with viral replication, so it has been postulated to be useful in preventing testicular damage and infertility.[10] Interferon alfa-2b may reduce the duration of symptoms and incidence of complications.[12][13] In cases of hydrocele formation, excess fluid can be removed.[10]
Prognosis[edit]
Prognosis for most people who experience mumps is excellent as long-term complications and death are rare. Hospitalization is typically not required.[4] Mumps is usually self-limiting and symptoms resolve spontaneously within two weeks as the immune system clears the virus from the body.[5][10] In high-risk groups such as immunocompromised persons, prognosis is considered to be the same as for other groups.[4] For most people, infection leads to lifelong immunity against future infection. Reinfections appear to be more mild and atypical than the first infection.[10] The overall case-fatality rate of mumps is 1.6–3.8 people per 10,000, and these deaths typically occur in those who develop encephalitis.[5]
Mumps orchitis typically resolves within two weeks. In 20% of cases, the testicles may be tender for a few more weeks. Atrophy, or reduction of size, of the involve testicle occurs in 30–50% of orchitis cases, which may lead to abnormalities in sperm creation and fertility such as low sperm count, absence of sperm in semen, reduced sperm motility, reduced fertility (hypofertility) in 13% of cases, and rarely sterility. Hypofertility can, however, occur in cases without atrophy. Abnormalities in sperm creation can persist for months to years after recovery from the initial infection, the length of which increases as the severity of orchitis increases. Examination of these cases shows decreased testicular volume, tenderness of the testicles, and a feeling of inconsistency when handling the testicles. Infertility is linked to severe cases of orchitis affecting both testes followe by testicular atrophy, which may develop up to one year after the initial infection. Of bilateral orchitis cases, 30–87% experience infertility. There is a weak association between orchitis and later development of epididymitis and testicular tumors.[5][10][12]
Mumps meningitis typically resolves within 3–10 days without long-term complications.[7] In meningoencephalitis cases, higher protein levels in CSF and a lower CSF glucose to blood glucose ratio are associated with longer periods of hospitalization.[16] Approximately 1% of those whose CNS is affected die from mumps.[11][17] Post-infectious encephalitis tends to be relatively mild, whereas post-infectious encephalomyelitis has a case-fatality rate of up to 10%.[17] Most cases of mumps deafness affect just one ear and are temporary, but permanent hearing loss occurs in 0.005% of infections.[5][13] Myocarditis and pericarditis that occur as a result of mumps may lead to endocardial fibroelastosis, i.e. thickening of the endocardium.[11][13] With extreme rarity, infertility and premature menopause have occurred as a result of mumps oophoritis.[5]
Prevention[edit]
Select mumps combination vaccines[1]
MMR(V)
MMR II Jeryl Lynn MMR
Morupar Urabe AM9 MMR
Priorix Jeryl Lynn RIT 4385 MMR
Trimovax Urabe AM9 MMR
Triviraten Rubini MMR
Priorix-Tetra Jeryl Lynn RIT 4385 MMRV
ProQuad Jeryl Lynn MMRV
Mumps is preventable with vaccination. Mumps vaccines use live attenuated viruses.[2] Most countries include mumps vaccination in their immunization programs, and the MMR vaccine, which also protects against measles and rubella, is the most commonly used mumps vaccine.[9] Mumps vaccination can also be done on its own[28] and as a part of the MMRV vaccine, which also provides protection against measles, rubella, chickenpox, and shingles. More than 120 countries have adopted mumps vaccination, but coverage remains low in most African, South Asian, and Southeast Asian countries.[25] In countries that have implemented mumps vaccination, significant declines in mumps cases and complications caused by infection such as encephalitis have been observed.[9] Mumps vaccines are typically administered in early childhood, but may also be given in adolescence and adulthood if need be.[7][25][29] Vaccination is expected to be capable of neutralizing wild-type MuVs not included in the vaccine since they do not appear to escape from vaccine-derived immunity.[14]
A variety of virus strains have been used in mumps vaccines, including the Jeryl Lynn (JL), Leningrad-3, Leningrad-3-Zagreb (L-Zagreb), Rubini, and Urabe AM9 strains. Some other less prominent strains exist that are typically confined to individual countries. These include the Hoshino, Miyahara, Torii, and NK M-46 strains that have been produced in Japan and the S-12 strain, which is used by Iran.[1][30] Mild adverse reactions are relatively common, including fever and rash,[7] but aseptic meningitis also occurs at varying rates.[1][30] Other rare adverse reactions include meningoencephalitis, parotitis, deafness from inner ear damage, orchitis, and pancreatitis.[17] Safety and effectiveness vary by vaccine strain:[1][30]
Rubini is safe but because of its low effectiveness in outbreaks, its use has been abandoned.
JL is relatively safe and has a relatively high effectiveness. The effectiveness is, though, is significantly lower in outbreaks. A modified version of JL vaccines is RIT 4385, which is also considered safe.
Urabe and Leningrad-3 are both at least as about as effective as JL but are less safe.
L-Zagreb, a modified version of Leningrad-3, is considered safe and effective, including in outbreaks.
Mumps protection from the MMR vaccine is higher after two doses than one[31] and is estimated to be between 79% and 95%, lower than the degree of protection against measles and rubella. This, however, has still been sufficient to nearly eliminate mumps in countries that vaccinate against it as well as significantly reduce frequencies of complications among the vaccinated.[14] If at least one dose is received, then hospitalization rates are reduced by an estimated 50% among the infected.[25] Compared to the MMR vaccine, the MMRV vaccine appears to be less effective in terms of providing mumps protection.[32] A difficulty in assessing vaccine effectiveness is that there is no clear correlate of immunity, so it is not possible to predict if a person has acquired immunity from the vaccine.[14]
There is a lack of data on the effectiveness of a third dose of the MMR vaccine. In an outbreak in which a third dose was administered, it was unclear if it had any effect on reducing disease incidence, and it only appeared to boost antibodies in those who previously had little or no antibodies to mumps.[14] Contraindications for mumps vaccines include prior allergic reaction to any ingredients or to neomycin, pregnancy, immunosuppression, a moderate or severe illness, having received a blood product recently, and, for MMRV vaccines specifically, a personal or familial history of seizures.[7] It is also advised that women not become pregnant in the four weeks after MMR vaccination.[29] No effective prophylaxis exists for mumps after one has been exposed to the virus, so vaccination or receiving immunoglobulin after exposure does not prevent progression to illness.[7][10][11]
For people who are infected or suspected to be infected, isolation is important in preventing the spread of the disease.[3][29] This includes abstaining from school, childcare, work, and other settings in which people gather together. In health care settings, it is recommended that health care workers use precautions such as face masks to reduce the likelihood of infection and to abstain from work if they develop mumps. Additional measures taken in health care facilities include reducing wait times for mumps patients, having mumps patients wear masks, and cleaning and disinfecting areas that mumps patients use.[29] The virus can be inactivated by means of formalin, ether, chloroform, heat, or ultraviolet light.[7]
Epidemiology[edit]
Mumps is found worldwide.[2] In the absence of vaccination against mumps, as occurred before vaccination was introduced, there are between 100 and 1,000 cases per 100,000 people each year, i.e. 0.1% to 1% of the population are infected each year. The number of cases peaks every 2–5 years,[9] with incidence highest in children 5–9 years old.[13] According to seroconversion surveys done prior to the start of mumps vaccination, a sharp increase in mumps antibody levels at age 2–3 was observed. Furthermore, 50% of 4–6 year olds, 90% of 14–15 year olds, and 95% of adults had tested positive to prior exposure to mumps, indicating that nearly all people are eventually infected in unvaccinated populations.[1][5]
Prior to the start of vaccination, mumps accounted for 10% of meningitis cases and about a third of encephalitis cases.[7] Worldwide, mumps is the most common cause of inflammation of the salivary glands.[6] In children, mumps is the most common cause of deafness in one ear in cases when the inner ear is damaged.[5] Asymptomatic infections are more common in adults,[9] and the rate of asymptomatic infections is very high, up to two-thirds, in vaccinated populations. Mumps vaccination has the effect of increasing the average age of the infected in vaccinated populations that have not previously experienced a mumps outbreak.[25] While infection rates appear to be the same in males and females, males appear to experience symptoms and complications, including neurological involvement, at a higher rate than females.[1][15] Symptoms are more severe in adolescents and adults than in children.[17]
It is common for outbreaks of mumps to occur. These outbreaks typically occur in crowded spaces where the virus can spread from person to person easily, such as schools, military barracks, prisons, and sports clubs.[1][10] Since the introduction of vaccines, the frequency of mumps has declined dramatically, as have complications caused by mumps. The epidemiology in countries that vaccinate reflects the number doses administered, age at vaccination, and vaccination rates. If vaccine coverage is insufficient, then herd immunity may be unobtainable and the average age of infection will increase, leading to an increase in the prevalence of complications. Risk factors that have been identified include age, exposure to a person with mumps, compromised immunity, time of year, travel history, and vaccination status.[1] Mumps vaccination is less common in developing countries, which consequently have higher rates of mumps.[15]
Cases peak in different seasons of the year in different regions. In temperate climates, cases peak in winter and spring, whereas in tropical regions no seasonality is observed.[25] Additional research has shown that mumps increases in frequency as temperature and humidity increase. The seasonality of mumps is thought to be caused by several factors: fluctuation in the human immune response due to seasonal factors, such as changes in melatonin levels; behavior and lifestyle changes, such as school attendance and indoor crowding; and meteorological factors such as changes in temperature, brightness, wind, and humidity.[1]
According to Chinese medical literature, mumps was recorded as far back as 640 B.C.[13] The Greek physician Hippocrates documented an outbreak on the island of Thasos in approximately 410 B.C. and provided a fuller description of the disease in the first book of Epidemics in the Corpus Hippocraticum.[5][33] In modern times, the disease was first described scientifically in 1790 by British physician Robert Hamilton in Transactions of the Royal Society of Edinburgh.[34] During the First World War, mumps was one of the most debilitating diseases among soldiers.[35] In 1934, the etiology of the disease, the mumps virus, was discovered by Claude D. Johnson and Ernest William Goodpasture. They found that rhesus macaques exposed to saliva taken from humans in the early stages of the disease developed mumps. Furthermore, they showed that mumps could then be transferred to children via filtered and sterilized, bacteria-less preparations of macerated monkey parotid tissue, showing that it was a viral disease.[5][33]
In 1945, the mumps virus was isolated for the first time. Just a few years later, in 1948, an inactivated vaccine using killed viruses had been invented. This vaccine only provided short-term immunity and was later discontinued and replaced in the 1970s with vaccines that have live but weakened viruses, which are more effective at providing long-term immunity than the inactivated vaccine. The first of these vaccines was Mumpsvax, licensed on 30 March 1967, which used the Jeryl Lynn strain. Maurice Hilleman created this vaccine using the strain taken from his then five-year-old daughter, Jeryl Lynn. Mumpsvax was later recommended for use in 1977, and the Jeryl Lynn strain continues to be used in vaccines today.[24][33]
Hilleman worked to combine the attenuated mumps vaccines with measles and rubella vaccines, creating the MMR-1 vaccine. In 1971, a newer version, MMR-2, was approved for use by the US Food and Drug Administration.[24] In the 1980s, countries started recognizing the benefit of receiving multiple doses, so a two-dose immunization schedule was widely adopted.[24][30] Including MMR-2, five MMR vaccines have been created since the 1960s, the others being Triviraten, Morupar, Priorix, and Trimovax. Since the mid-2000s, two MMRV vaccines have been in use: Priorix-Tetra and ProQuad.[1]
The United States of America began to vaccinate against mumps in the 1960s, with other countries following suit.[5] From 1977 to 1985, 290 cases per 100,000 people were diagnosed each year worldwide.[10] Although few countries recorded mumps cases after they began vaccination, those that did reported dramatic declines. From 1968 to 1982, cases declined by 97% in the USA, in Finland cases were reduced to less than 1 per 100,000 people per year,[25] and a decline from 160 cases per 100,000 to 17 per 100,000 per year in England was observed from 1989 to 1995.[31] By 2001, there had been a 99.9% reduction in the number of cases in the USA and similar near-elimination in other vaccinating countries.[5]
In Japan in 1993, concerns over the rates of aseptic meningitis following MMR vaccination with the Urabe strain prompted the removal of MMR vaccines from the national immunization program, resulting in a dramatic increase in the number of cases.[1][5] Japan now provides voluntary mumps vaccination separately from measles and rubella.[28] Starting in the mid-1990s, controversies surrounding the MMR vaccine emerged. One paper connected the MMR vaccine to Crohn's disease in 1995, and another in 1998 connected it to autism spectrum disorders and inflammatory bowel disease. These papers are now considered to be fraudulent and incorrect, and no association between the MMR vaccine and the aforementioned conditions has been identified. Despite this, their publication led to a significant decline in vaccination rates, ultimately causing measles, mumps, and rubella to reemerge in places with lowered vaccination rates.[10][12][33]
Notable outbreaks in the 21st century include more than 300,000 cases in China in 2013[13] and more than 56,000 cases in England and Wales in 2004–2005. In the latter outbreak, most cases were reported in then 15–24 year olds who were attending colleges and universities. This age group was thought to be vulnerable to infection because of the MMR vaccine controversies when they were to be vaccinated and due to MMR vaccine shortages that had also occurred at that time.[10] Similar outbreaks in densely crowded environments have frequently occurred in many other countries, including the USA, the Netherlands, Sweden, and Belgium.[24]
Resurgence[edit]
Select mumps outbreaks exceeding 1,000 cases in vaccinating locations[24]
2005–2006 Czech Republic 5,998
2006 USA 6,584
2009 New York (USA) 1,521
2009–2011 Jerusalem 3,130
2012–2013 Belgium 4,061
2013 Poland 2,436
2016–2017 Arkansas (USA) 2,706
In the 21st century, mumps has reemerged in many places that vaccinate against it, causing recurrent outbreaks. These outbreaks have largely affected adolescents and young adults in densely crowded spaces, such as schools, sports teams, religious gatherings, and the military, and it is expected that outbreaks will continue to occur. The cause of this reemergence is subject to debate, and various factors have been proposed, including waning immunity from vaccination, low vaccination rates, vaccine failure, and potential antigenic variation of the mumps virus.[1][5][24][25]
Waning immunity from vaccines is likely the primary cause of the mumps resurgence. In the past, subclinical natural infections provided boosts to immunity similar to vaccines. As time went on with vaccine use, these asymptomatic infections declined in frequency, likely leading to a reduction in long-term immunity against mumps. With less long-term immunity, the effects of waning vaccine immunity became more prominent, and vaccinated individuals have frequently fallen ill from mumps. A third dose of the vaccine provided in adolescence has been considered to address this as some studies support this. Other research indicates that a third dose may only be useful for short-term immunity in responding to outbreaks,[14][24] which is recommended for at-risk persons by the Advisory Committee on Immunization Practices of the Centers for Disease Control and Prevention.[1]
Low vaccination rates have been implicated as the cause of some outbreaks in the UK, Canada, Sweden, and Japan, whereas outbreaks in other places, such as the USA, the Czech Republic, and the Netherlands, have occurred mainly among the vaccinated. Compared to the measles and rubella vaccines, mumps vaccines appear to have a relatively high failure rate, varying depending on the vaccine strain. This has been addressed by providing two vaccine doses, supported by recent outbreaks among the vaccinated having primarily occurred among those who only received one dose. Lastly, certain mumps virus lineages are highly divergent genetically from vaccine strains, which may cause a mismatch between protection against vaccine strains and non-vaccine strains, though research is inconclusive on this matter.[1][24]
The word "mumps" is first attested circa 1600 and is the plural form of "mump", meaning "grimace", originally a verb meaning "to whine or mutter like a beggar". The disease was likely called mumps in reference to the swelling caused by mumps parotitis, reflecting its impact on facial expressions and the painful, difficult swallowing that it causes. "Mumps" was also used starting from the 17th century to mean "a fit of melancholy, sullenness, silent displeasure".[10][36] Mumps is sometimes called "epidemic parotitis".[4][8][13]
^ a b c d e f g h i j k l m n o p q r Su SB, Chang HL, Chen AK (5 March 2020). "Current Status of Mumps Virus Infection: Epidemiology, Pathogenesis, and Vaccine". Int J Environ Res Public Health. 17 (5): 1686. doi:10.3390/ijerph17051686. PMC 7084951. PMID 32150969.
^ a b c d e f g h Davison P, Morris J (13 August 2020). "Mumps". NCBI. StatPearls. PMID 30521206. Retrieved 30 October 2020.
^ a b Levine DA (December 2016). "Vaccine-Preventable Diseases In Pediatric Patients: A Review Of Measles, Mumps, Rubella, And Varicella". Pediatr Emerg Med Pract. 13 (12): 1–20. PMID 27893360. Retrieved 30 October 2020.
^ a b c d e f g h i Kutty PK, Kyaw MH, Dayan GH, Brady MT, Bocchini JA, Reef SE, Bellini WJ, Seward JF (15 June 2010). "Guidance for isolation precautions for mumps in the United States: a review of the scientific basis for policy change". Clinical Infectious Diseases. 50 (12): 1619–1628. doi:10.1086/652770. PMID 20455692.
^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP (January 2015). "Molecular biology, pathogenesis and pathology of mumps virus". J Pathol. 235 (2): 242–252. doi:10.1002/path.4445. PMC 4268314. PMID 25229387. Retrieved 30 October 2020.
^ a b c d Kessler AT, Bhatt AA (15 November 2018). "Review of the Major and Minor Salivary Glands, Part 1: Anatomy, Infectious, and Inflammatory Processes". J Clin Imaging Sci. 8: 47. doi:10.4103/jcis.JCIS_45_18. PMC 6251248. PMID 30546931.
^ a b c d e f g h i j k "Mumps". Centers for Disease Control and Prevention (CDC). CDC. Retrieved 30 October 2020.
^ a b c d "Mumps". National Center for Biotechnology Information. A.D.A.M. Medical Encyclopedia. Archived from the original on 17 October 2014. Retrieved 30 October 2020.
^ a b c d e f g h i j k l m "Mumps virus nomenclature update: 2012" (PDF). Wkly Epidemiol Rec. 87 (22): 217–224. 1 June 2012. PMID 24340404. Retrieved 30 October 2020.
^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad Davis NF, McGuire BB, Mahon JA, Smyth AE, O'Malley KJ, Fitzpatrick JM (April 2010). "The increasing incidence of mumps orchitis: a comprehensive review". BJU Int. 105 (8): 1060–1065. doi:10.1111/j.1464-410X.2009.09148.x. PMID 20070300. S2CID 20761646. Retrieved 30 October 2020.
^ a b c d e f g h i j k l m Gupta RK, Best J, MacMahon E (14 May 2005). "Mumps and the UK epidemic 2005". BMJ. 330 (7500): 1132–1135. doi:10.1136/bmj.330.7500.1132. PMC 557899. PMID 15891229.
^ a b c d e f g h i Masarani M, Wazait H, Dinneen M (November 2006). "Mumps orchitis". J R Soc Med. 99 (11): 573–575. doi:10.1258/jrsm.99.11.573. PMC 1633545. PMID 17082302.
^ a b c d e f g h i j k l m n o Shu M, Zhang YQ, Li Z, Liu GJ, Wan C, Wen Y (18 April 2015). "Chinese medicinal herbs for mumps". Cochrane Database Syst Rev. 2015 (4): CD008578. doi:10.1002/14651858.CD008578.pub3. PMC 7198052. PMID 25887348.
^ a b c d e f g h i j Latner DR, Hickman CJ (7 May 2015). "Remembering mumps". PLOS Pathog. 11 (5): e1004791. doi:10.1371/journal.ppat.1004791. PMC 4423963. PMID 25951183. Retrieved 30 October 2020.
^ a b c d e f g h i j k Junghanss T (2013). Manson's tropical diseases (23rd ed.). Oxford: Elsevier/Saunders. p. 261. ISBN 978-0-7020-5306-1. Archived from the original on 13 May 2016. Retrieved 30 October 2020.
^ a b Kanra G, Isik P, Kara A, Cengiz AB, Seçmeer G, Ceyhan M (December 2004). "Complementary findings in clinical and epidemiologic features of mumps and mumps meningoencephalitis in children without mumps vaccination". Pediatr Int. 46 (6): 663–668. doi:10.1111/j.1442-200x.2004.01968.x. PMID 15660864. S2CID 43534364.
^ a b c d e f g h i j Senanayake SN (20 October 2008). "Mumps: a resurgent disease with protean manifestations". Med J Aust. 189 (8): 456–459. doi:10.5694/j.1326-5377.2008.tb02121.x. PMID 18928441. S2CID 13771290. Retrieved 30 October 2020.
^ Smatti MK, Cyprian FS, Nasrallah GK, Al-Thani AA, Almishal RO, Yassine HM (19 August 2019). "Viruses and Autoimmunity: A Review on the Potential Interaction and Molecular Mechanisms". Viruses. 11 (8): 762. doi:10.3390/v11080762. PMC 6723519. PMID 31430946.
^ "ICTV Taxonomy history: Mumps orthorubulavirus". International Committee on Taxonomy of Viruses (ICTV). ICTV. Retrieved 30 October 2020.
^ Cox RM, Plemper RK (June 2017). "Structure and organization of paramyxovirus particles". Curr Opin Virol. 24: 105–114. doi:10.1016/j.coviro.2017.05.004. PMC 5529233. PMID 28601688.
^ Rima B, Balkema-Buschmann A, Dundon WG, Duprex P, Easton A, Fouchier R, Kurath G, Lamb R, Lee B, Rota P, Wang L (December 2019). "ICTV Virus Taxonomy Profile: Paramyxoviridae". J Gen Virol. 100 (12): 1593–1954. doi:10.1099/jgv.0.001328. PMC 7273325. PMID 31609197. Retrieved 30 October 2020.
^ a b c Najjar FE, Schmitt AP, Dutch RE (7 August 2014). "Paramyxovirus glycoprotein incorporation, assembly and budding: a three way dance for infectious particle production". Viruses. 6 (8): 3019–3054. doi:10.3390/v6083019. PMC 4147685. PMID 25105277. Retrieved 30 October 2020.
^ a b c Harrison MS, Sakaguchi T, Schmitt AP (September 2010). "Paramyxovirus assembly and budding: building particles that transmit infections". Int J Biochem Cell Biol. 42 (9): 1416–1429. doi:10.1016/j.biocel.2010.04.005. PMC 2910131. PMID 20398786.
^ a b c d e f g h i Ramanathan R, Voigt EA, Kennedy RB, Poland GA (18 June 2018). "Knowledge gaps persist and hinder progress in eliminating mumps". Vaccine. 36 (26): 3721–3726. doi:10.1016/j.vaccine.2018.05.067. PMC 6031229. PMID 29784466.
^ a b c d e f g h Beleni AI, Borgmann S (31 July 2018). "Mumps in the Vaccination Age: Global Epidemiology and the Situation in Germany". Int J Environ Res Public Health. 15 (8): 1618. doi:10.3390/ijerph15081618. PMC 6121553. PMID 30065192. Retrieved 30 October 2020.
^ Skrha J, Stepan J, Sixtova E (October 1979). "Amylase isoenzymes in mumps". Eur J Pediatr. 132 (2): 99–105. doi:10.1007/BF00447376. PMID 499265. S2CID 28963086.
^ "Amylase Test". Lab Tests Online. Archived from the original on 29 March 2009. Retrieved 30 October 2020.
^ a b "Changes in the Immunization Schedule Recommended by the Japan Pediatric Society" (PDF). Japan Pediatric Society. Japan Pediatric Society. 1 August 2018. Retrieved 30 October 2020.
^ a b c d "Mumps Clinical Information – Minnesota Dept. of Health". Archived from the original on 19 May 2011. Retrieved 30 October 2020.
^ a b c d Peltola H, Kulkarni PS, Kapre SV, Paunio M, Jadhav SS, Dhere RM (15 August 2007). "Mumps outbreaks in Canada and the United States: time for new thinking on mumps vaccines". Clin Infect Dis. 45 (4): 459–466. doi:10.1086/520028. PMID 17638194. Retrieved 30 October 2020.
^ a b Demicheli V, Rivetti A, Debalini MG, Pietrantonj CD (15 February 2012). "Vaccines for measles, mumps and rubella in children". Cochrane Database Syst Rev. 2012 (2): CD004407. doi:10.1002/14651858.CD004407.pub3. PMC 6458016. PMID 22336803.
^ Ma SJ, Li X, Xiong YQ, Yao AL, Chen Q (November 2015). "Combination Measles-Mumps-Rubella-Varicella Vaccine in Healthy Children: A Systematic Review and Meta-analysis of Immunogenicity and Safety". Medicine (Baltimore). 94 (44): e1721. doi:10.1097/MD.0000000000001721. PMC 4915870. PMID 26554769.
^ a b c d "Tracing the story of mumps: a timeline". Pharmaceutical Technology. Pharamaceutical Technology. Retrieved 30 October 2020.
^ Hamilton R (1790). "IX. An Account of a Distemper, by the common People in England vulgarly called the MUMPS". Transactions of the Royal Society of Edinburgh. 2 (2): 59–72. doi:10.1017/S0263593300027280. PMC 5550187. PMID 29139995. Retrieved 30 October 2020.
^ Van-Way CW, Marble WS, Thompson G. "Diseases in World War I". The United States World War I Centennial Commission. United States Foundation for the Commemoration of the World Wars. Retrieved 30 October 2020.
^ "mumps (n.)". Etymonline. Online Etymology Dictionary. Retrieved 30 October 2020.
ICD-10: B26
ICD-9-CM: 072
eMedicine: emerg/324 emerg/391 ped/1503
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Actor Danny Trejo is expanding his taco empire with a new restaurant in Hollywood called Trejo's Cantina. The restaurant, which opened Monday, is next to Big Wangs, at the corner of Selma Avenue and Cahuenga Boulevard.
This is the second restaurant for Trejo, film producer Ash Shah and Jeff Georgino. The trio opened Trejo's Tacos on La Brea Avenue earlier this year, and launched a Trejo's food truck a couple of weeks ago. The truck makes an appearance at every Rams home game.
Like the original Trejo's Tacos, the cantina has plenty of tacos, including a rainbow cauliflower taco with cashew cream and a black pepper tofu taco with pickled onions. Trejo actually happens to be particularly fond of tofu. (There's meat on the menu too).
"We're trying to talk healthy," said Trejo. "Me being the character I play on TV, you wouldn't think I like tofu and kale, but I do. It's really good for you."
Chef John-Carlos Kuramoto, who has cooked at Michael's in Santa Monica and Osteria Mozza and who became executive chef of Trejo's restaurants four months ago, wanted to add larger entrées. New additions include a grilled spice-rubbed half Jidori chicken; marinated hanger steak and charred branzino. Each is served with tortillas made specifically for the restaurant by La Princesita in Boyle Heights and grilled vegetables.
"I wanted to expand the menu but stay true to our philosophy of keeping things simple," said Kuramoto. "We're making as much as possible in-house, including the hot sauce and salsas."
There's also a kale salad — Trejo loves kale too — with pomegranates, manchego cheese and a citrus vinaigrette, and a butter lettuce salad with charred tomato and summer squash.
Kuramoto said he's also frequenting the Hollywood farmers market and plans to make use of the produce in some of the specials.
"I'm trying to get away from the idea of quick service and create a place where you can stay and just hang out," said the chef.
With the larger location, which offers more seating than the restaurant on La Brea Avenue, there's a full bar with cocktails by Mark Hendrix, including a michelada, a mezcal Negroni, spiked horchata and a margarita with a mango and serrano chile shrub, tequila, lime and agave. There are also 34 beers on tap, mostly from local breweries.
The two Trejo's restaurants also have a beer made for them by Boomtown Brewery in the downtown L.A. Arts District. It's a German-style lager with what partner Shah calls "Mexican elements" in the form of corn and flaked rice.
With two concepts complete, Shah isn't ruling out the possibility of more Trejo's restaurants.
"We didn't want it to be a cookie-cutter thing," said Shah. "For the next one, maybe a taqueria."
Trejo's Cantina is open daily from 11 a.m. to 9 p.m. Shah said they plan on extending the hours to 2 a.m. on the weekends, and may add a breakfast service as well.
1556 N. Cahuenga Ave., Los Angeles, (323) 461-TACO, www.trejostacos.com.


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Main Runway - ROSTERS POSTED!
Your fledgling modeling agency has just been given a remarkable opportunity: the chance to represent the most successful runway models for the Spring/Summer 2018 runway season. After months of scouting, fashion week is nearly upon us and the time to finalize your runway roster is approaching rapidly.
As an agent, you must select 18 models to represent your agency on the runway. For every show one of your signed models walks in, you will be paid a designated amount, depending on the caliber and prestige of the show.
Your team of 18 girls will comprised of three girls from three categories of models.
This season you will be guaranteed your first TWO catwalk queens, TWO muses, and FOUR fresh faces, so choose wisely! Once your first 8 models have been assigned, we will randomly select an order for agents and go through each list, assigning models in order of preference.
But - a model can only be shared by THREE to FIVE agencies MAX (depending on how many sign up), so if you really want a certain girl, make sure to put her HIGH on your preference list to increase the odds of getting her! This overlap limit will not apply for the models in your guaranteed slots.
If four agencies have already signed a certain model, you are not allowed to swap for her.
DON'T FORGET TO FILL OUT THE FORM ABOVE FOR TEAM SELECTION SINCE NEW YORK FASHION WEEK IS FAST APPROACHING! THE DEADLINE FOR SIGNING UP IS THURSDAY FEBRUARY 8th!
Be sure to get your model picks in ASAP! We don't have long for sign-ups so we'll have to post teams on Friday after fashion week officially starts. Sorry this game is so last minute!


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