Freddy Turner

Frederick George Turner dit Freddy Turner, né le à Port Elizabeth en Afrique du Sud et mort le à Johannesburg, est un joueur de rugby à XV qui a joué avec l’équipe d’Afrique du Sud. Il évolue au poste d’ailier mais il joue également pour les Springboks au poste de centre, d’arrière.

Freddy Turner évolue avec l’ Eastern Province qui dispute la Currie Cup, puis avec le Transvaal jerseys stores. Il dispute à 19 ans son premier test match le contre les Wallabies wusthof meat tenderizer. Il joua son dernier test match contre les Lions britanniques le . De 1933 à 1938, il dispute 11 matchs sur les 13 que disputent les Springboks. Les Wallabies effectuent leur première tournée en Afrique du Sud en 1933 pour une série de cinq test matchs. Freddie Turner inscrit 1 essai. Les Springboks gagnent la série par 3 victoires à 2. Ce sont leur premières confrontations. En 1937, les Springboks rendent visite d’abord aux Wallabies (2-0), puis les Springboks remportent leur série contre les All Blacks (2-1) lors d’un passage en Nouvelle-Zélande how do you tenderise steak. Les All Blacks remportent le premier test match mais s’inclinent lors des deux suivants. Ils ont affaire à forte partie car cette équipe d’Afrique du Sud de 1937 est parfois décrite comme la meilleure qui ait joué en Nouvelle-Zélande. Freddie Turner inscrit 2 essais contre les All Blacks et joue les trois rencontres. En 1938 les Lions britanniques sont en Afrique du Sud. Deux victoires et une défaite laissent une nouvelle fois les Springboks vainqueurs finaux. Freddie Turner inscrit 1 essai, 4 transformations, 3 pénalités contre les Lions britanniques et joue les trois rencontres.

Tereshchenko diamond

The Tereshchenko Diamond, sometimes known as the Tereshchenko Blue, is a 42.92 carat diamond of blue colour that is cut in the pear shape. The diamond is rare, belonging to the Type IIb diamond, and believed to originate from India. The Tereshchenko diamond is the second biggest blue diamond in the world. Shaped by Cartier for a private order by the Tereshchenko family battery operated fabric shaver. The diamond is in the rare Type IIb diamond.

Originally owned by the Russian aristocrats the Tereshchenko family.

Like the Hope Diamond, the blue diamond “Tereshchenko” was found in India, near Golconda cheap goalkeeper gloves uk, in Kollur mine in the Guntur district of Andhra Pradesh (which at the time was part of the Golconda kingdom), in the seventeenth century.

The original owner of the diamond is the Tereshchenko family.

The diamond weighted 150 carats before the cut and was secretly brought from India especially for Mikhail Tereshchenko running pouch for keys.[citation needed] The “Tereshchenko Diamond” is the world’s largest blue diamond and is the second largest diamond to the “Hope”, which belonged to the French crown.[citation needed] However, after the French Revolution, the diamond went to England and the United States. This blue diamond was cut in France in 1673, it weighed 67 carats and was also referred to a very rare Type IIb diamond.[citation needed] After the cut the blue diamond “Hope” weighed 44 carats.

After the Cartier cut, “The Tereshchenko Blue” weighed 42.92 carats. It had an ideal form of cut – a “pear” shape. The Tereshchenko diamond took its place in the classification of the rarest Type IIb diamond. The jeweler from the Place Vendôme in Paris, made it the centerpiece of necklace, where harmoniously conjoined forty-six intoxicating imagination diamonds, weighing from 0.13 to 2.88 carats with cut of all kinds of shapes: “marquis”, round, “pear”, “heart” and variety of colors: pale yellow, lemon, aqua, Persian green, golden-yellow, grey, blue, purple, pink, bright orange and bright yellow. This necklace will remain one of the biggest orders in the history of the House of Cartier.

According to legend,[citation needed] these two stones Hope Diamond and Tereshchenko Diamond with the same deep blue radiance, in the late nineteenth and early twentieth century, were stolen from the eyes of a sculpted statue of the goddess Sita, the wife of Rama, the seventh Avatar of Vishnu, and were then shipped to Europe. This legend is used to explain the tragic events in the life of Mikhail Tereshchenko, the Tereshchenko family and Russia after Mikhail became the owner of the gem. However, much like the “curse of Tutankhamun”, this general type of “legend” was most likely the invention of Western authors during the Victorian era.

Rowborough Manor

Rowborough Manor (also Rodeberge, 11th century; Rowberg, 13th century; Rotirburgh, 14th century; Rowbarho, 16th century) is a manor house in the parish of Brading on the Isle of Wight.

Rowborough lies between Hardingshute Manor and Hill Manor. From the fact that it was held of the Confessor by the Abbot of St. Swithun’s, Winchester, as an alod it may be inferred that it was included in the 50 hides at Brading reputed to have been granted to the monastery by Ine king of the West Saxons. In 1086 it was in the possession of William son of Azor. The overlordship followed the same descent as Yaverland to the Russells, John Rivers (de Riperiis) being their tenant at the end of the 13th century. The estate afterwards came to Ralph de Olne, but had lapsed before 1346 to the overlords

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, the Russells, and subsequently followed the same descent as Yaverland until 1846. It was then sold with the other estates of the Wright family, the purchaser being Sir William Oglander

Timeline: History of Football Pads

Football pads were first used in 1877, not long after football became an established pastime on U.S. college campuses. The first football pads were much smaller and thinner than those used in today’s games. Over time, football pads evolved to cover more of the body, stand up to rough use and to be lighter and sturdier than the original pads.
In 1877, Princeton football player L.P. Smock designed the first football pads. Smock’s pads were thin quilted layers sewn to the shoulders, thighs and knees of the laced-up jersey and knee pants he designed as the first football uniform for Princeton’s players. The pads were not very heavy, and they also did not provide much protection.
The 1890s saw significant changes in football rules and the creation of better football pads. In 1894, the “flying wedge” formation was outlawed after it killed 20 collegiate players and injured 100 more in a single season. Meanwhile, sports equipment manufacturers, including Spalding and Victor, began marketing leather football pads. The pads were thicker than Smock’s original pads, and their leather construction made them more sturdy. Also, unlike Smock’s pads, the leather pads were designed to be sewn or strapped to the outside of the football uniform.
In 1915, sports equipment manufacturers developed and sold the first football helmets. These helmets were made of soft leather and were designed primarily to cover and protect the ears. Although early football helmets were called “head harnesses” by their manufacturers, their distinctive earflaps soon earned them the nickname “dog-ear helmets.” In the 1930s, the first hard leather helmets appeared, followed by rigid plastic helmets in the 1950s.
In the 1930s

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, football shoulder pads first took on the form we recognize today: a separate set of pads that cover the entire shoulder and upper chest area. The pads were first developed by the Spalding company and were made primarily of leather. Like some shoulder pads used today, they had laces in the front so players could adjust the fit. Although they offered greater protection than the quilted or leather pads, they were also significantly heavier.
During the 1980s, football padding and helmets continued to improve. Helmets developed full face masks that prevented injuries like broken noses. Manufacturers began to make shoulder pads using plastic and other synthetic materials that made the padding lighter and stronger. In addition, shoulder pads began to use a cantilevered design that dissipated the impact of a hit. Hip, thigh and knee pads also became common equipment. Today, college and professional football players are required to wear a helmet and pads when they play.

Philippine Council of Evangelical Churches

The Philippine Council of Evangelical Churhces (PCEC) is an organization of more than seventy Evangelical and Mainline Protestant churches, and more than 210 para-church organizations in the Philippines. It is a member of the World Evangelical Alliance. In 2010, the Philippine census by the National Statistics Office found that 2.68 percent of the population in the Philippines are Evangelical Christians affiliated with the PCEC, making it the third largest religious denomination in the Philippines after the Roman Catholic Church (80.6%) and Islam (5.6%), respectively. The PCEC was estimated to represent close to eleven million adherents as of 2011.

The PCEC was established as a small umbrella organization in 1965. To date compare electric shavers, it is the largest organization of Christian denominations in the Philippines thermos stainless steel.

A transformed nation through the discipling of every Filipino for the Lord Jesus Christ.

To glorify God by catalyzing the multiplication of evangelical churches that will transform their communities to become Christ-centered.

Мои дорогие

мелодрама

Ярослав Лупий

Вера Кудрявцева

Любовь Соколова
Люсьена Овчинникова
Владимир Меньшов

Геннадий Карюк
Виктор Крутин

Леонид Афанасьев

Одесская киностудия

67 мин.

СССР СССР

русский

1975

«Мои дорогие» (укр. Любі мої) — мелодрама 1975 года о жизни в деревне.

Фильм рассказывает о судьбе четырёх сестёр-доярок, проживающих в одной из советских деревень в середине 1970-х годов.

Тут и старшая Антонида, которой пришлось после смерти матери расстаться с любимым человеком и воспитывать троих младших сестёр where to buy football shirts, и которую они поэтому до сих пор ласково называют няней tempered glass bottles.

Тут и Шура, чей муж по работе постоянно разъезжает по стране и зовёт её каждый раз с собой, но которая не хочет покидать любимую деревню и в итоге уговаривает мужа остаться с ней.

Тут и Лида, которая, по-видимому, из-за породы Петровых постоянно рожает мужу только дочерей, несмотря на то, что он страстно желает парня.

Тут и младшая Маша, которая полностью замкнулась после смерти своего мужа-военного два года назад и поэтому постоянно даёт отпор ухаживающему за ней Володе.

Бывший любимый человек Антониды стал теперь известным певцом и выступает по телевидению. Удастся ли ей встретиться с ним вновь…

Blauhals-Schnellläufer

Blauhals-Schnellläufer

Der Blauhals-Schnellläufer, auch Bunter Schnellläufer (Diachromus germanus) ist ein Käfer aus der Familie der Laufkäfer und der Unterfamilie der Harpalinae.

Der Gattungsname Diachromus ist von altgr. διά diá „hindurch“ und χρῶμα chrōma „Farbe“ abgeleitet. Der Artname germanus (lat.) bedeutet „deutsch“ oder „Bruder“. Über die Bedeutung der beiden Namen lässt sich nur spekulieren. Der Namensteil „Blauhals“ bezieht sich auf den blaugrünen Halsschild, der Name „Schnellläufer“ wird häufig für Arten der Unterfamilie Harpalinae gebraucht.

Der Käfer wird acht bis zehn Millimeter groß. Er hat einen breiten Kopf mit nach vorn gerichteten Mundwerkzeugen, einen herzförmigen Halsschild und gestreifte Flügeldecken. Diese verbreitern sich nach hinten über zwei Drittel ihrer Länge wenig und enden dann gemeinsam halbkreisförmig abgerundet. Kurz vor dem Ende sind die Seiten der Flügeldecken leicht wellenförmig ausgerandet. Die Oberseite ist kurz abstehend behaart. Die Färbung ist unverwechselbar. Kopf, Beine, Fühler und der größte Teil der Flügeldecke sind rotgelb, auf beiden Flügeldecken gemeinsam befindet sich am Ende ein großer dunkler, bläulicher Fleck. Der Halsschild ist bis auf den feinen Seitenrand intensiv blaugrün.

Kopf und Halsschild sind dicht mittelstark, die Flügeldecken dicht fein punktiert how do i tenderize meat. Auf dem Kopf sitzt nur eine Borste (Supraorbitalseta) auf jeder Seite etwas hinter der Mitte des Oberrandes der dunklen Augen. Diese treten mäßig hervor. Die Fühler sind elfgliedrig, fadenförmig und ab der zweiten Hälfte des dritten Glieds behaart (Abb. 1)

Die fünfgliedrigen Tarsen der Vorderbeine und des mittleren Beinpaares sind bei den Männchen verbreitert (Abb. 2) und auf der Unterseite bürstenartig behaart. Das erste Hintertarsenglied ist so lang wie das zweite und dritte zusammen.

Die Käfer leben phytophag, sie fressen vorzugsweise unreife Grassamen. Man findet die Art in der Ebene und niederen Gebirgslagen, häufig gesellig unter Steinen. Die wärmeliebende Art wird von Waldrändern, Gärten, Feldern und Ruderalflächen gemeldet, vor allem auf Sandboden.

Die Art hat ihr Verbreitungszentrum im Mittelmeergebiet, die nördliche Grenze des Verbreitungsareals verläuft durch Deutschland, wo man seit Beginn der achtziger Jahre ein Vordringen nach Norden beobachtet. Außerdem ist die Art aus den Niederlanden, Dänemark, Großbritannien, dem Kaukasus und Westasien bekannt.

Heinz Freude, Karl Wilhelm Harde best running hydration, Gustav Adolf Lohse: Die Käfer Mitteleuropas. Band 2. Adephaga 1. Elsevier, Spektrum, Akad. Verl., München 1976, ISBN 3-87263-025-3.

The 5 Worst Pieces of Fitness Advice

Go outside and ride your bike.
That¡¯s what my mom would say when I complained about being fat as a kid.
She wasn¡¯t completely wrong. If I wanted to lose weight, riding my bike more wouldn¡¯t hurt.
But I took her words as gospel, and for decades I equated exercise with weight loss, fooling myself into believing that I could eat like a pig as long as I was active. (Example: I used to make Doritos-and-ketchup sandwiches on white bread as an after-school snack. Don¡¯t you dare mock me! They are fantastic.)
I did as mom said and rode my bike around our suburban neighborhood. I ran track and played on multiple sports teams in high school. In college I walked 20-30 minutes to class every day, played pickup games, and ruled intramural sports. After graduation I regularly hit the gym five times a week.
Yet, despite all that effort, I still looked like a Nutrisystem ¡°before¡± photo.
Finally, in my 30s, I tried P90X, a high-intensity workout program that comes with a recommended diet. Following its guidelines, I shrunk my meal portions, stopped eating packaged and processed foods, and cut out alcohol. And I lost 35 pounds.
Sure, the workouts helped, but intense exercise was nothing new to me. It was the diet that finally knocked off the weight.
My point is that we all receive bad fitness advice, often from well-meaning people: parents, coaches, friends, bros at the gym getting so ripped, bro. If you¡¯re like me, some of that bad advice sticks. But it shouldn¡¯t. Here are five pieces of lousy, outdated fitness advice to ignore.
Not true.
This is what people who sell exercise equipment and workout programs want you to think. If you really want to shed pounds, you must get your diet in check. Exercise is good¡ªthe benefits are many¡ªbut losing weight is about putting fewer calories in your Chalupa-hole.
For those who prefer hard science: When researchers from Hunter College recently studied the Hadza hunter/gatherer tribe in Tanzania, and compared its lifestyle to the typical Western lifestyle, they found no difference in energy expenditures between the two.
So whether you hunt birds and pick berries all day, or sit in an office cubicle, your body burns about the same amount of calories. In other words, obesity is not caused by inactivity. It¡¯s a calories-in problem.
THE TRUTH: If you want to lose weight, eating healthier foods and ingesting fewer calories is key. To give yourself an edge, find a weight-loss buddy. According to a study published in the journal Obesity, people who attempt to slim down together can significantly influence each other¡¯s results. This helps explain why husbands and wives who attend programs such as WeightWatchers together regularly have success.
¡°Come on! Three more! You can do it! Push!¡± We¡¯ve all heard these ¡°words of encouragement¡± in the weight room.
My high school football buddies used to shout them as I struggled to eek out one last bench press during team training sessions. As a bonding experience, and a willpower test, these workouts had value. But they set a terrible precedent. I equated pain with gain and discounted any workout that didn¡¯t leave my body in agony.
¡°No pain, no gain is a bad strategy for lifelong exercise,¡± says Dr. Michael Otto, author of Exercise for Mood and Anxiety: Proven Strategies for Overcoming Depression and Enhancing Well-Being. If you¡¯re not an elite athlete and you¡¯re exercising for the health benefits, including better heart health, improved mood, weight regulation, increased energy, or getting more sleep, there is no need for pain. You can attain all of these benefits with minimal discomfort. Plus, a painful workout is one you are less likely to repeat.
THE TRUTH: Moderate exercise for 40 minutes, four to five times a week, is all you need to glean the health benefits of exercise, Otto says. Walking, jogging, dancing, swimming, volleyball, touch football, and shooting baskets all count as ¡°moderate exercise.¡± Even some common chores meet the requirements. For a list of moderate exercises and the length of time they should be done, copy and paste this URL into your browser (after you finish this article, of course): http://www.nhlbi.nih.gov/health/public/heart/obesity/lose_wt/phy_act.htm.
About five years ago

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, I bought myself a set of adjustable dumbbells. I kept the weight low and went high-rep. Why? Because I didn¡¯t want big, bulky arms. What I wanted were¡ªand I¡¯d heard this phrase for years¡ªlong, lean muscles.
Well, I was an idiot.
Shane Doll, a personal trainer in Charleston, S.C., says he laughs when companies advertise the ability to sell someone the means to long, lean muscles.
¡°There has always been a misconception that weightlifting and resistance training will make you big and bulky,¡± Doll says. ¡°What nobody thinks about is that, from a pure anatomical standpoint, the idea of making your muscles longer is impossible. The joint distance never changes. The physiology behind that is pretty simple yet they think, ¡®Pilates or this machine will make my muscles long and sleek.¡¯¡±
If the marketing was true, people who did Pilates would look like Plastic Man.
THE TRUTH: Whether it¡¯s Pilates or pushups, the adaptation of the muscle tissue does not change. Muscle bulk only happens with intense workouts coupled with protein and/or other supplements.
To get the lean, toned look of a swimmer (in the absence of swimming, of course), Doll recommends using a variety of resistance exercises, completed in fast-paced circuits that use burst training principals, which are short bursts of high-intensity effort. Reps should be in the 8-20 range, or work in sets of 30 seconds on, 30 seconds off. By varying the number of repetitions, rest periods, exercises, and other variables in your workout, you¡¯ll continue to develop or maintain a lean physique without reaching a plateau.
No, you probably don¡¯t.
When I was doing P90X, on the nights before the very challenging plyometric workout, I would gorge on pasta because that¡¯s what I thought you were supposed to do before an intense workout. Once again, I was wrong.
¡°Unless you¡¯re going to physically exert yourself for more than 90 minutes the next day, you really don¡¯t need to think about carbo-loading,¡± says Nancy Clark, RD, author of Nancy Clark¡¯s Sports Nutrition Guidebook.
THE TRUTH: To prepare for a big event, the best strategy is to continue eating your normal, healthy sports diet (a plate filled with two-thirds grain, starches, veggies, and fruits, and one-third protein) while cutting back on training, Clark says. ¡°By taking a rest day, your muscles have the time they need to store those carbs that you eat instead of burning them off in yet another workout.¡±
This is one reason why high school, college, and NFL teams have easy practices the day before a game. Besides letting aches and pains heal, athletes¡¯ bodies are able to store carbs for energy.
I have friends who swear that working out in the morning is better because it boosts your metabolism all day, increases your energy, and gives you a natural high that carries into the afternoon.
I also have friends who say that night is the best time to work out because you can burn off all of the calories you consumed that day, plus you¡¯re so tired at the end that it¡¯s easier to fall asleep.
Who¡¯s right?
When it comes to fat loss, there¡¯s not much of a benefit either way, Doll says. And while minor details like when you work out, what time you take your whey protein, etc. are great for Internet debate, they ultimately don¡¯t make a big enough difference to matter. What happens over a 24-hour period is what truly matters.
¡°I¡¯ve seen too many of the ¡®rules¡¯ be broken, and people still see great results. Hard work, adequate rest/recovery, and consistency with clean nutrition are 95 percent of the equation for most,¡± Doll says. ¡°Elite athletes and bodybuilders can make an argument that the last five percent is pretty important, but this is far from something the average Joe or Jane should concern themselves with. The big picture gets lost in the details.¡±
THE TRUTH: The best time to work out is whenever you most feel like exercising and/or can fit it into your schedule, Dr. Otto says. ¡°There is some research suggesting that the time of day you work out may give you better performance should you also compete at that time, but these effects are subtle.¡±
If you want to get a little more specific, follow these simple guidelines from Doll, who has been a trainer for 20 years:
1. Avoid high-intensity training (burst training, interval training) later in the evening, as it produces chemicals in the brain that can make it difficult to fall asleep and can disrupt natural circadian rhythms.
2. The best time for weight training is when your maximum effort can be exerted.
3. Avoid exercising shortly after eating a meal. If you train in the morning, eat a small amount of whey protein or a piece of fruit as a pre-workout snack. Digestion should be kept to a minimum.
If you¡¯ve been eating and working out based on advice you received so long ago you can¡¯t remember where it came from, question it. When it comes to working out, conventional wisdom changes as quickly as the science, which is still discovering how the human body works.

Bacteriophage T12

Bacteriophage T12 is a bacteriophage that infects the bacterial species Streptococcus pyogenes, and converts a harmless strain of bacteria into a virulent strain. It carries the speA gene which codes for erythrogenic toxin A. speA is also known as streptococcal pyogenic exotoxin A, scarlet fever toxin A, or even scarlatinal toxin. Note that when the term ‘spe’A is italicized, the reference is to the gene. In contrast, when the term ‘spe’A is not italicized, the toxin itself is being referred to. Erythrogenic toxin A converts a harmless, nonvirulent strain of Streptococcus pyogenes to a virulent strain through lysogeny, a life cycle which is characterized by the ability of the genome to become a part of and be stably maintained in the host cell for generations. Phages with a lysogenic life cycle are also called temperate phages. A virulent strain of bacteria is one that is “extremely infective” and causes medical, clinical symptoms. Bacteriophage T12, a member of a family of related speA-carrying bacteriophages, is also a prototypic phage for all the speA-containing phages of Streptococcus pyogenes, meaning that its genome is the prototype for the genomes of all such phages of S.pyogenes. It is the main suspect as the cause of Scarlet Fever, an infectious disease that affects small children.

The possibility of bacteriophage involvement in speA production was first introduced in 1926 when Cantacuzene and Boncieu reported that nonvirulent strains of S.pyogenes were transformed to virulent strains through some transferable element. Frobisher and Brown reported similar results in 1927, and in 1949, the reports were confirmed by Bingel Later, in 1964, Zabriskie reported that phage T12 could cause speA production by lysogeny in strains that it became a part of. In 1980, Johnson, Schlievert and Watson were able to confirm this and show that the gene for speA production was transferred from toxigenic strains of bacteria to non-toxigenic strains through lysogeny. In their experiment, every transformed, toxin-producing bacterial colony was lysogenic, i.e. contained the T12 gene. In addition, none of the colonies containing the T12 genome was negative for speA, and therefore, the conclusion was drawn that all lysogens produced the toxin. However, McKane and Ferretti reported, in 1981, that a mutant of phage T12 induced speA production virulently. This mutant, the bacteriophage T253, entered the lytic cycle, a life cycle in which the host cell is destroyed. In 1983, Johnson and Schlievert published a map of the T12 genome, revealing also that three rounds of packaging occur in the genome. The very next year, Johnson and Schlievert and Weeks and Ferreti also found, independently, that the bacteriophage T12 carries the structural gene for speA. In 1986, Johson, Tomai and Schlievert mapped the attachment site (attP) for T12 adjacent to the speA gene, and established that all bacterial strains producing the toxin carry either phage T12 itself, or a closely related bacteriophage. And finally, in 1997, McShan and Ferretti published that they had found the second attachment site (attR) for T12, while also revealing in another publication, which was also credited to Tang

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, that bacteriophage T12 inserts into a gene that encodes a serine tRNA in the host.

The physical map of the T12 genome was found to be circular with a total length of 36.0kb. The phage genome is reported to carry the speA gene, which is a 1.7kb segment of the phage T12 genome flanked by SalI and HindIII sites.

The phage integrase gene (int) and the phage attachment site (attp) are located just upstream of the speA gene in the phage genome. The bacteriophage T12 integrates into S. pyogenes chromosome by site-specific recombination into the anticodon loop of a gene that codes for serine tRNA. The bacterial attachment site (attB) has a 96 base pair sequence homologous to the phage attachment site and is located at the 3’ end of the tRNA gene such that the coding sequence of the tRNA gene remains intact after integration of the prophage. Phage T12 is the first example of a phage from a gram-positive, low G-C content host that uses this kind of integration site.

Diseases like Scarlet Fever and Streptococcal toxic shock syndrome are caused by lysogenized streptococcal strains that produce speA. The diseases are systemic responses to the speA circulating within the body.

Scarlet fever, also known as scarletina, is so called because of the characteristic bright red rash it causes. It is most common in children between four and eight years of age.

The first stage of scarlet fever is typically strep throat (streptococcal pharyngitis) characterized by sore throat, fever, headache and sometimes nausea and vomiting. In two to three days, this is followed by the appearance of a diffuse erythematous rash that has a sandpaper texture. The rash first appears on the neck, then spreads to the chest

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, back and body extremities. A yellowish white coating covers the tongue, and is later shed, leaving the tongue with a strawberry appearance and swollen papillae. The rash fades away after five to six days of the onset of the disease, and is followed by peeling of skin, particularly over the hands and feet.

Penicillin, an antibiotic, is the drug of choice for the treatment of scarlet fever as for any other S. pyogenes infection. For those who are allergic to penicillin, the antibiotics erythromycin or clindamycin can be used. However, occasional resistance to these drugs has been reported.

In Streptococcal toxic shock syndrome (StrepTSS), speA produced by infected streptococcal strains acts as a superantigen and interacts with human monocytes and T lymphocytes, inducing T-cell proliferation and production of monokines (e.g. tumor necrosis factor α, interleukin 1, interleukin 6), and lymphokines (e.g. tumor necrosis factor β, interleukin 2, and gamma-interferon).These cytokines(TNFα, TNFβ) so produced seems to mediate the fever, shock and organ failure characteristic of the disease.

Strep TSS is an acute, febrile illness that begins with a mild viral-like syndrome characterized by fever, chills, myalgia, diarrhea, vomiting and nausea and involves minor soft-tissue infection that may progress to shock, multi-organ failure, and death.

While penicillin is an effective treatment of mild infection, it is less effective in a severe case. Emerging treatments for strep TSS include clindamycin and intravenous gamma-globulin.

The presence of lysogenic bacteriophage T12 can be tested through plaque assays if the indicator strain utilized is susceptible to the phage being tested. Plaque assays consist of pouring a soft agar solution with an indicator strain onto an agar plate. The indicator strain should be a strain of bacteria that can be infected by the phage that needs to be detected. After the soft agar is set the samples that are being tested for phage presence are then spread-plated onto the soft agar plates. The plates are then incubated overnight and checked for clearings (plaques) the next day. If the phage is present, indicator strains will become infected and go through the normal lysogenic cycle while the plates incubate, and then undergo lysis. The plaque that determines whether the phage is present or not is caused by the lysis of the indicator strains. Titers of plaques can be found by diluting the samples and counting plaque-forming units (PFUs).

Biochemical tests such as southern blots can also be used to detect the speA that the phage produces from the speA gene. This was done in research by Johnson, Tomai and Schlievert in 1985 by isolating the DNA of Streptococcal strains and running a restriction digest using BglII. After the digest was complete, the DNA samples were run on gel to separate the DNA. The DNA from this gel was then transferred to nitrocellulose paper and incubated with probes specific for speA. An image of this southern blot can be seen in this article.

Bacteriophages are very robust biological agents, are very hard to kill, and are very easily spread. Ultraviolet light can enhance the production of both phage T12 and speA. However, this is only to a point. UV light stresses lysogenic bacteria, causing them to propagate and burst the host bacterial cells. In the case of T12, exposure to UV light increases the propagation of bacteriophage T12 at 20 seconds of exposure. After 20 seconds of exposure the UV light starts to kill the bacteriophage by damaging its genome.

ITC Enschede

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The International Institute for Geo-Information Science and Earth Observation (ITC) was an institute of higher (tertiary) education located in Enschede, Netherlands. As of 1 January 2010 it has been incorporated into the University of Twente as the sixth faculty

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, while preserving its unique international character as a faculty sui generis, and is now formally known as University of Twente, Faculty of Geo-Information Science and Earth Observation (ITC).

ITC was founded in 1950 with the name International Training Centre for Aerial Survey by the former Prime Minister of the Netherlands, Prof Orange Runner Waist Pack. Dr. Willem Schermerhorn to provide training in map making as an aid to developing countries. Over the years its mission has been adjusted to changing technological and development realities

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, so that today it offers MSc, Master’s, Diploma and Certificate courses in Geo-information Science (GIS) and Earth Observation (EO) with emphasis on applications in developing countries. ITC promotes PhD Research in collaboration with universities in the Netherlands. In addition, ITC undertakes applied and technological consultancy projects world wide and contributes to fundamental research in the fields of its expertise.

More than 19,000 students from over 170 countries have followed ITC courses since 1950. The institute’s degrees are accredited by the Dutch system of higher education.

ITC offers degree, diploma and certificate courses in geo-information science and earth observation applied to eight domains: Disaster management Yellow Women Dresses; Earth sciences; Geoinformatics; Governance; Land administration; Natural resources; Urban planning; and Water resources.

ITC has several joint educational programmes with partner institutes in the developing world, for example joint MSc programmes in geo-hazards with the Indian Institute of Remote Sensing in Dehradun, India and Gadjah Mada University in Yogyakarta, Indonesia. It also offers much of its curriculum as distance education modules, and offers custom training courses to meet specific capacity building requirements, both in Enschede and abroad.