Vasa

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Vasa

(vä`zə), Pol. Waza, royal dynasty of Sweden (1523–1654) and Poland (1587–1668). Gustavus IGustavus I
, 1496–1560, king of Sweden (1523–60), founder of the modern Swedish state and the Vasa dynasty. Known as Gustavus Eriksson before his coronation, he was the son of Erik Johansson, a Swedish senator and follower of the Sture family.
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, founder of the dynasty in Sweden, was succeeded by his sons Eric XIVEric XIV,
1533–77, king of Sweden (1560–68), son and successor of Gustavus I. To strengthen the power of the crown, he limited (1561) the privileges of the royal dukes.
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 (reigned 1560–68) and John III (reigned 1568–92). John III married the sister of Sigismund II of Poland, and their son was elected (1587) king of Poland as Sigismund IIISigismund III,
1566–1632, king of Poland (1587–1632) and Sweden (1592–99). The son of John III of Sweden and Catherine, sister of Sigismund II of Poland, he united the Vasa and Jagiello dynasties.
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. On John's death Sigismund succeeded to the Swedish throne, but his Catholicism led to his deposition (1599) in Sweden, where his uncle Charles IXCharles IX,
1550–1611, king of Sweden (1604–11), youngest son of Gustavus I. He was duke of Södermanland, Närke, and Värmland before his accession. During the reign of his brother, John III (1568–92), he opposed John's leanings toward Catholicism.
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 (reigned 1604–11) succeeded him. The house was thus split into a senior Catholic line (in Poland) and a cadet Protestant line (in Sweden), and the two lines engaged in chronic warfare. Charles IX of Sweden was succeeded by Gustavus IIGustavus II
(Gustavus Adolphus), 1594–1632, king of Sweden (1611–32), son and successor of Charles IX. Military Achievements

Gustavus's excellent education, personal endowments, and early experience in affairs of state prepared him for his crucial role
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; on Gustavus's death (1632) his daughter ChristinaChristina
, 1626–89, queen of Sweden (1632–54), daughter and successor of Gustavus II. From her father's death (1632) until 1644 she was under a regency headed by Chancellor Axel Oxenstierna.
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 ascended the throne. With Christina's abdication (1654) in favor of her first cousin, Charles X, the Swedish throne passed to the ZweibrückenZweibrücken
, Fr. Deux-Ponts, city (1994 pop. 35,704), Rhineland-Palatinate, W Germany, near the Saarland border. Zweibrücken is a transportation center and has ironworks, steelworks, and factories that produce leather goods, wood products, machines, and
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 line of the house of Wittelsbach. In Poland, Sigismund III was succeeded (1632) by his son Ladislaus IVLadislaus IV,
1595–1648, king of Poland (1632–48), son and successor of Sigismund III. His reign was marked by struggles with his subjects and wars with the Swedes, the Russians, and the Ottomans.
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, who was succeeded (1648) by his brother John IIJohn II
(John Casimir), 1609–72, king of Poland (1648–68), son of Sigismund III. He was elected to succeed his brother, Ladislaus IV. The turbulent period of his reign is known in Polish history as the Deluge.
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. John abdicated in 1668.

Vasa

 

Swedish royal dynasty (1523-1654). The founder was Gustavus I Vasa (ruled 1523-60). His sons Eric XIV (1560-68) and John III (1568-92), his grandson Sigismund (1592-1604, in actuality until 1599), Gustavus’ son Charles IX (1604-11), Charles’ son Gustavus II Adolphus (1611-32), and the daughter of Gustavus II, Christina (1632-54) were all monarchs of Sweden. The Vasa dynasty also reigned in Poland from 1587 to 1668, including Sigismund III (1587-1632), who was the son of John III of Sweden and Catherine Jagello, the daughter of the Polish king Sigismund I the Old (with the election of Sigismund III as king of Sweden in 1592, the Swedish-Polish personal union that lasted until 1599 was established); and the sons of Sigismund III Ladislas IV (1632-48) and John Casimir (1648-68).

References in periodicals archive ?
Real time PCR analysis of the stem cell markers DDX4 and SSEA-4, which are potent germ cell markers as well, could be clearly detected in PGC like cells, whereas the primary hUCM-SC cell populations showed only faint staining for these markers.
In addition to measuring the size distribution of cfsRNA and detecting full-length transcripts, we further investigated the integrity of cfsRNA by quantifying the amounts of 5', middle, and 3' regions of ACTB and DDX4 transcripts via RT-qPCR analysis of 9 semen samples.
4 mL seminal plasma at each time point and then quantified each region of the ACTB and DDX4 transcripts by RT-qPCR.
To observe the effect of Triton X-100 on the stability of cfsRNA, we also added Triton X-100 (Sigma-Aldrich) to 5 other seminal samples and quantified the 5' region of ACTB and DDX4 mRNAs at different time points.
We then extracted the RNA from 400 [micro]L of the filtered and unfiltered aliquots of seminal plasma and quantified the 5' region of the ACTB and DDX4 mRNAs.
Short PCR amplicons (<240 bp; see Table 1 in the online Data Supplement) targeting different regions of the ACTB and DDX4 transcripts were detected in cfsRNA samples from all 9 volunteers; however, we detected long PCR amplicons of ACTB mRNA (1499 bp) in 2 of the 9 volunteers but detected no long amplicons for DDX4 mRNA (1909 bp).
We further evaluated the integrity of cfsRNA by quantifying the amounts of the 3 different regions of ACTB and DDX4 transcripts.
Given that cfsRNA exists mainly in partially degraded forms and that human semen is known to contain various ribonucleases (25), we tested the stability of cfsRNA by a time-course analysis of different regions of the ACTB and DDX4 transcripts.
4, A and B, revealed no significant changes in seminal ACTB mRNA or DDX4 mRNA concentrations after filtration through a 5-[micro]m filter, suggesting that these mRNA transcripts were not contained within intact cells.
3%, respectively, of the 5' region of ACTB mRNA and could not amplify any DDX4 mRNA (Fig.
Detection of full-length transcripts was rare, and the quantitative analysis of multiple regions of seminal mRNAs showed preferential degradation of the 3' region for both ACTB and DDX4, indicating that exonucleases were primarily involved in the degradation of cfsRNA.
The 3' region of DDX4, however, was scarcely detectable and underwent more rapid degradation.