ライフサイエンスコーパス: Sv

1 ly low volume transport between 5.0 and 10.0 Sv.

2 MBq/kg (0.110 mCi/kg) is approximately 0.01 Sv for females and males.

3 during Heinrich event 4 and to average 0.029 Sv over all episodes.

4 SMA I&T were 0.12 +/- 0.07 and 0.05 +/- 0.03 Sv/GBq, respectively.

5 177)Lu-PSMA I&T were 0.12 0.07 and 0.05 0.03 Sv/GBq, respectively.

6 alivary glands, 0.7 Sv for kidneys, and 0.05 Sv for red marrow that are composed of 99.4% alpha, 0.5%

7 that would lead to an effective dose of 0.1 Sv in the first year.

8 .0 cm/s and a volume transport of 1.65 Sv (1 Sv = 1 x 10(6) m(3)/s).

9 ulf Stream transports approximately 31 Sv (1 Sv = 10(6) m(3) s(-1)) of water and 1.3 x 10(15) W of he

10 overflow into the SCS of 0.84 +/- 0.39 Sv (1 Sv = 10(6) m(3) s(-1)), a significant linear upward tren

11 arges to be as high as 0.13 sverdrup (Sv) (1 Sv = 1 million cubic meters per second) during Heinrich

12 ed value of up to 30 to 40 sverdrups (Sv) (1 Sv = 10(6) cubic meters per second), and it occurs mainl

13 l overturning in which about 20 sverdrups (1 Sv = 10(6) m(3) s(-1)) upwell in the Southern Ocean, wit

14 erdrups (Sv) (range: 4.0 to 34.9 Sv, where 1 Sv = a flow of ocean water of 10(6) cubic meters per sec

15 MATERIALS AND C3(1) Sv-40 large T antigen transgenic mice (n = 23) were stud

16 icrotumors receive high doses (>20 Gy or 100 Sv [relative biological effect = 5]).

17 Infection of adult 129 Sv/Ev mice with consensus Sindbis virus strain TR339 is

18 In adult 129 Sv/Ev mice, subcutaneous inoculation with 100 PFU of TR3

19 n vitro in peritoneal exudate cells from 129 Sv/Ev versus IFN-alpha/betaR(-/-) mice.

20 infection or IFN-alpha/beta treatment in 129 Sv/Ev and TD-derived BMDC but not in virus-infected or I

21 y comparing the pathogenesis of TR339 in 129 Sv/Ev mice and alpha/beta interferon receptor null (IFN-

22 t impaired in ERK1-/- mice on the inbred 129 Sv and C57BL/6 backgrounds.

23 to screen a BAC library containing mouse 129 Sv/Ev genomic DNA.

24 regulation in BMDCs derived from normal 129 Sv/Ev, IFNAR1-/-, and TD mice following infection with S

25 d conducted in vivo studies in syngeneic 129 Sv/Ev, C57BL/6, and conditional knockout mice with Rora

26 ed survival of Slc7a7Lbu/Lbu mice on the 129 Sv/Ev x C57BL/6 F2 background, but postnatal growth fail

27 Wild-type 129-Sv-Ev mice (129 mice) and IFN-gamma receptor knockout mi

28 129/Sv embryonic stem cells, transfected with DNA containing

29 and FcgammaRIII expression in C57BL/6J, 129/Sv, and C57BL/6J x 129/Sv mice.

30 Interestingly, I-mfa-null embryos on a 129/Sv background had no placental defect, generally survive

31 in model (Arg52Gly, Nkx2-5(+/R52G)) in a 129/Sv background was analyzed by histopathology, surface, a

32 (Refs 6,7) increases TGCT frequency on a 129/Sv background.

33 We generated a murine model in a 129/Sv genetic background by knocking-in an Nkx2-5 homeodoma

34 In a 129/Sv genetic background, TF null embryos do not survive be

35 ncy of LOH, whereas Trp53(+/-) mice on a 129/Sv or (C57BL/6 x 129/Sv) mixed background have a very lo

36 y EAE course in C57BL6/J mice carrying a 129/Sv-derived interval on chromosome 17.

37 ime crypt development was completed, all 129/Sv epithelial cells were lost.

38 ice in two backgrounds: C57BL/6 (B6) and 129/Sv (129) hybrids (B6-129) and inbred B6.

39 eptor heterozygous mutant mice on B6 and 129/Sv backgrounds (B6IR x 129IR) and performed a genome-wid

40 ssion patterns in wild-type C57BL/6J and 129/Sv mice.

41 othionein (MT)-knockout (MT-KO) mice and 129/Sv wild-type (WT) controls at 4 mg/kg induced hepatic TN

42 .e., C57BL/6 and BALB/c for GKO mice and 129/Sv//Ev for RGKO mice).

43 To examine the in vivo function of APC, 129/Sv embryonic stem (ES) cells were transfected with DNA e

44 dult C57Bl/6-ROSA26 left and right arrow 129/Sv chimeric mice.

45 SGK1 expression is also increased in B-129/Sv-4A11(+/+) mice and paralleled increases seen for NCC.

46 B-129/Sv-4A11(+/+) mice display an 18% increase of plasma pota

47 under control of its native promoter (B-129/Sv-4A11(+/+)) develop hypertension (142 +/- 8 versus 113

48 ngiotensinogen are increased 2-fold in B-129/Sv-4A11(+/+), and blockade of the ANGII receptor type 1

49 ndicate that the use of mixed background 129/Sv x C57BL/6 mice to study effects of gene deletions in

50 t mice with the same genetic background (129/Sv//Ev mice).

51 through cooperative interactions between 129/Sv(Id-1) and B6 ROSA26/+ cells.

52 port that mixed background p21-deficient 129/Sv x C57BL/6 mice showed increased in vitro and in vivo

53 ghly polymorphic, germ-line competent F1(129/Sv-+Tyr+p x CAST/Ei) mouse embryonic stem cell line was

54 and GKO mice did not differ from female 129/Sv//Ev controls in either mortality or reactivation.

55 Forty 129/Sv female mice (64-68 weeks old), 20 wild type (WT) and

56 ocess of contig construction clones from 129/Sv and C57BL/6J BAC libraries were isolated.

57 e marrow-derived mast cells (BMMCs) from 129/Sv mice showed more robust degranulation upon the engage

58 '-methylcholanthrene (MCA) sarcomas from 129/Sv mice.

59 Analyses of adult B6 <--> 129/Sv mice indicated that forced expression of E-cadherin s

60 itors present in developing B6-ROSA26<-->129/Sv chimeras.

61 testinal epithelium of C57Bl/6-ROSA26<-->129/Sv chimeric mice led to precocious differentiation of so

62 the small intestine of C57Bl/6-ROSA26<->129/Sv mice.

63 Analyses of adult B6-ROSA26<-->129/Sv-APC chimeric mice revealed that forced expression of

64 Male and female homozygous 129/Sv mice carrying four copies of the human cytochrome P45

65 s in locomotion, we generated F2 hybrid (129/Sv x C57BL/6) D2 dopamine receptor (D2R)-deficient mice

66 ate in humans, and ablation of PDGF-C in 129/Sv background mice results in death during the perinatal

67 n vivo, we generated Akr1b7(-/-) mice in 129/Sv background.

68 ily kinase Lyn enhanced degranulation in 129/Sv BMMCs but inhibited this response in C57BL/6 cells.

69 f Apc and Axin, and induced apoptosis in 129/Sv but not in neighboring B6-ROSA26 epithelial cells.

70 53 and p21 were significantly reduced in 129/Sv cathepsin K(-/-) OCs and forced expression of catheps

71 h high basal Fyn and Stat5 expression in 129/Sv cells, which was not reduced by TGF-beta1 treatment.

72 Introduction of genes targeted in 129/Sv embryonic stem (ES) cells into NOD mice brings about

73 Lef-1/beta-cat was expressed in 129/Sv embryonic stem cell-derived small intestinal epitheli

74 did increase c-Kit-mediated migration in 129/Sv mast cells.

75 etinal folds in adult B6 mice but not in 129/Sv mice homozygous for a p53 null mutation.

76 clinical disease and was more common in 129/Sv mice than in 129/Sv x C57BL/6 animals.

77 ce results in a milder phenotype than in 129/Sv mice, and we present a phenotypic characterization of

78 with neither isotype being protective in 129/Sv mice.

79 d was more common in 129/Sv mice than in 129/Sv x C57BL/6 animals.

80 viously reported that deletion of p21 in 129/Sv x C57BL/6 mixed genetic background mice induced a sev

81 null mutant than in control mice: 11% in 129/Sv//Ev controls, 50% in GKO mice (P = 0.0002), and 33% i

82 ngth mouse P2X3 gene from a phage lambda-129/Sv genomic library.

83 alyzed in an intercross between the lean 129/Sv mouse strain and the obesity-prone EL/Suz mouse strai

84 alpha(E) deficiency in mice with a mixed 129/Sv x BALB/c background, but not in mice further backcros

85 f the nephrin-deficient CNF mouse model: 129/Sv-Nphs1(tm1Rkl)/J.

86 suggestive evidence for additional novel 129/Sv resistance QTL on Chr 5 and 17 and susceptibility on

87 than mice with wild-type NQO1 (NQO1+/+; 129/Sv background strain).

88 ns junctions and basolateral surfaces of 129/Sv (DeltaN89 beta-catenin) intestinal epithelial cells a

89 1-2% of 129/Sv (DeltaN89 beta-catenin) villi exhibited an abnormal b

90 n contrast, on the genetic background of 129/Sv mice, the same mutation causes severe hyperinsulinemi

91 ing in an independently derived stock of 129/Sv x C57BL/6 p21(-/-) mice.

92 In contrast, 14% of 129/Sv x C57BL/6 TF-deficient embryos escape this early mort

93 somic strain') in which chromosome 19 of 129/Sv+/+ was replaced by its MOLF-derived homologue.

94 he BALB/c background, but not C57Bl/6 or 129/Sv, suggests a genetic predisposition toward mammary tum

95 s efficiently as those from the parental 129/Sv strain.

96 ptibility in the genetically predisposed 129/Sv inbred mouse strain.

97 coordinated control of these processes, 129/Sv embryonic stem (ES) cells, transfected with a recombi

98 in Th1-prone C57BL/6, but not Th2-prone 129/Sv mice.

99 tial for embryonic viability in the pure 129/Sv background but the presence of C57BL/6 alleles yields

100 ptible B6 mice for GzmB and in resistant 129/Sv mice for GzmA and/or the GzmB cluster, point to granz

101 arly-stage infection, innately resistant 129/Sv mice were also tested.

102 ocompatibility complex (Mhc) from strain 129/Sv (haplotype bc).

103 progeny of crosses between mouse strains 129/Sv and C3H/HeJ.

104 velops, the highly nephritis-susceptible 129/Sv and DBA/1 mice exhibited significantly increased urin

105 iency of Apobec1 on the TGCT-susceptible 129/Sv inbred background to determine whether dosage of Apob

106 The 129S1/SvImJ (129/Sv) inbred strain of mice is an excellent model for stud

107 Investigators targeting 129/Sv genes mapping within chromosomal regions reported her

108 e male mice of the three strains tested: 129/Sv//Ev wild type, gamma interferon (IFN-gamma) knockout

109 Our data indicated that 129/Sv cathepsin K(-/-) osteoclasts (OCs) lacked normal apop

110 In this study, we report that 129/Sv mice had high levels of circulating IgE, increased ex

111 ressed in the haploid spermatid and that 129/Sv Sprm-1(-/-) mice are subfertile when compared with wi

112 rived H2b congenic MRL/lpr mice from the 129/Sv (H2b) strain.

113 e acts as a genetic modifier between the 129/Sv and C57BL/6 strains.

114 ed cathepsin K(-/-) mouse strains in the 129/Sv and C57BL/6J backgrounds and found that, only in the

115 backgrounds and found that, only in the 129/Sv background, cathepsin K(-/-) mice exhibit many charac

116 essential earlier in development on the 129/Sv background.

117 utation (Rac1Asn17) was expressed in the 129/Sv embryonic stem cell-derived component of the small in

118 taN89 beta-catenin) was expressed in the 129/Sv embryonic stem cell-derived component of the small in

119 roduced by Rac1Leu61 or Rac1Asn17 in the 129/Sv epithelium do not spread to adjacent normal C57Bl/6 e

120 Forced expression of Id-1 in the 129/Sv epithelium results in a decline in Id-2 and Id-3 to b

121 f E-cadherin may have helped prevent the 129/Sv gut epithelium from undergoing neoplastic transformat

122 B/c strain, these mice were carrying the 129/Sv haplotype of MHC (mMCP-6(-/-)/H-2bc).

123 sceptibility to spontaneous TGCTs on the 129/Sv inbred genetic background.

124 cell tumor (TGCT) susceptibility in the 129/Sv mouse model of human pediatric TGCTs.

125 ically to modulate susceptibility in the 129/Sv mouse model of spontaneous TGCTs, we discovered an un

126 compared with the much lower rate in the 129/Sv strain (5%).

127 re hyperinsulinemia, suggesting that the 129/Sv strain harbors alleles that interact with the insulin

128 t 89% of adult alpha(E)(-/-) mice on the 129/Sv x BALB/c background developed inflammatory skin lesio

129 ely active human Rac1 (Rac1Leu61) in the 129/Sv-derived small intestinal epithelium of C57Bl/6-ROSA26

130 enotype that spontaneously occurs in the 129/Sv-SlJ strain and is characterized by small eyes that la

131 ing progeny from backcrosses between the 129/Sv-Ter/+ and MOLF/Ei strains provided modest evidence th

132 ced the IFN-gamma null mutation into the 129/Sv//Ev background.

133 mice but in only a single neuron in the 129/Sv//Ev control mice.

134 knockout strains and was not seen in the 129/Sv//Ev control.

135 ate of the GKO and RGKO mice than of the 129/Sv//Ev males.

136 wo different mutant stat1 alleles in the 129/Sv/Ev background, we demonstrate that IFNR-dependent con

137 defensin-producing Paneth cells in their 129/Sv epithelium and also developed intestinal adenomas.

138 ration via gavage at a dose of 6 g/kg to 129/Sv mice induced hepatic TNF-alpha production in Kupffer

139 audal midbrain: a phenotype identical to 129/Sv-En1-/- mice.

140 Metallothionein-knockout and wild-type 129/Sv mice were pair-fed an ethanol-containing liquid diet

141 on of the Mif gene on a segregating B6 x 129/Sv background (MIF-KO) under ad libitum (AL) feeding and

142 IgG1-treated C57BL/6J x 129/Sv mice had significantly more pulmonary eosinophilia th

143 t IgG3-mediated protection in C57BL/6J x 129/Sv mice was associated with lower levels of IFN-gamma an

144 owever, we now report that in C57BL/6J x 129/Sv mice, IgG3 is protective while IgG1 is not protective

145 than IgG2a- and IgG3-treated C57BL/6J x 129/Sv mice.

146 -gamma expression in infected C57BL/6J x 129/Sv mice.

147 sion in C57BL/6J, 129/Sv, and C57BL/6J x 129/Sv mice.

148 rp53(+/-) mice on a 129/Sv or (C57BL/6 x 129/Sv) mixed background have a very low frequency of mammar

149 nsfer of the NOD H2(g7) haplotype onto 129S1/Sv, 310 females were produced by NOD x (NOD x 129.H2(g7)

150 Significant 129S1/Sv resistance contributions were identified on Chr 1, 15

151 C57BL/6J and 129S6/Sv (B6 and 129) mice differ dramatically in their suscep

152 s, and Pkd1(RC/RC) mice on a C57BL/6 x 129S6/Sv F1 background.

153 rains that are sensitive (CD-1, FVB/N, 129T2 Sv/EMS, and C57Bl/10).

154 eas in the KA-sensitive strains FVB/N, 129T2 Sv/EMS, and CD-1 were significantly larger at 56 days po

155 129X1/Sv mice, which do not mount a glucagon response to hypog

156 ce (FVB/N, C3H/He, Balb/cAnN, C57BL/6, 129X1/Sv) fed for three months (eight mice per strain) the est

157 3(-/-) mice but almost undetectable in 129X1/Sv Col4a3(-/-) mice.

158 vivo insulin secretion was greatest in 129X1/Sv mice, but the counter-regulatory response to hypoglyc

159 ntly slower on the C57BL/6 than on the 129X1/Sv background.

160 leukemia) mean dose ranged from 6.6 to 12.2 Sv.

161 at a rate of 8.4 0.7 Sv, composed of 4.5 0.3 Sv of well-ventilated Dense Shelf Water, and 3.9 0.5 Sv

162 ffectiveness of 5 revealed mean doses of 2.3 Sv for salivary glands, 0.7 Sv for kidneys, and 0.05 Sv

163 The Gulf Stream transports approximately 31 Sv (1 Sv = 10(6) m(3) s(-1)) of water and 1.3 x 10(15) W

164 water overflow into the SCS of 0.84 +/- 0.39 Sv (1 Sv = 10(6) m(3) s(-1)), a significant linear upwar

165 annual-average HSSW production rate of ~0.4 Sv (10(6) m(3) s(-1)), which we use to ground truth addi

166 requiring deep water advection of 1.1 - 6.4 Sv through Fram Strait.

167 ll-ventilated Dense Shelf Water, and 3.9 0.5 Sv of old Circumpolar Deep Water entrained into cascadin

168 style factors, and higher dose groups (> 0.5 Sv) generally driving the observed trends.

169 e-body, with a cumulative mean dose of < 0.5 Sv, or at a low dose rate (< 10 mSv/day).

170 ng can be monitored with a resolution of 1.5 Sv.

171 rculatory diseases combined ranged from 2.5%/Sv [95% confidence interval (CI): 0.8, 4.2] for France t

172 interval (CI): 0.8, 4.2] for France to 8.5%/Sv (95% CI: 4.0, 13.0) for Russia.

173 t not all, of the Dense Shelf Water (3.4 0.6 Sv) is generated on the continental shelves of the Wedde

174 points alone (which range from 4.2% to 5.6%/Sv for these populations).

175 y of 2.0 cm/s and a volume transport of 1.65 Sv (1 Sv = 1 x 10(6) m(3)/s).

176 ean doses of 2.3 Sv for salivary glands, 0.7 Sv for kidneys, and 0.05 Sv for red marrow that are comp

177 ] is exported northward at a rate of 8.4 0.7 Sv, composed of 4.5 0.3 Sv of well-ventilated Dense Shel

178 water transport-based calculations (8.4-9.7 Sv) yielding larger rates than tracer-based estimates (3

179 umes ranged from 2.4 to 11.2 and 2.9 to 21.9 Sv, respectively.

180 7 +/- 5.6 sverdrups (Sv) (range: 4.0 to 34.9 Sv, where 1 Sv = a flow of ocean water of 10(6) cubic me

181 r rates than tracer-based estimates (3.7-4.9 Sv).

182 ld-type and PPARalpha-null mice on either an Sv/129 or a C57BL/6N background were not markedly differ

183 and EPS enzymes was elevated in both Rv and Sv cells cultured in half-strength medium, compared to t

184 reporting through auditory feedback (Bleeper Sv; Vertec Scientific Ltd; Berkshire, UK) on patient dos

185 The effect of the Bleeper Sv device on operator radiation exposure was consistent

186 osure was significantly lower in the Bleeper Sv group.

187 use (n=253) or no use (n=252) of the Bleeper Sv radiation monitor.

188 GFR was predicted by Sv(PGBM/glom), AER, and sex.

189 used to determine alveolar surface density (Sv) and total volume of respiratory region (TVvr).

190 exposes more in-plane Sv while limiting edge Sv exposure, which is conducive to methanol synthesis.

191 m low to intermediate and to high blood flow/Sv(O(2)) (9.2 [6.2-10.9] vs. 8.3 [5.9-9.8] vs. 7.9 [6.5-

192 intraclass correlation coefficient (ICC) for Sv o2 and Spearman correlation for cardiac index.

193 y greater IFN-gamma compared with cells from Sv/129 (SLC11A1(-/-)) mice.

194 ce density of peripheral GBM per glomerulus [Sv(PGBM/glom)] (r = 0.50, P < 0.001) and Vv(Mes/glom) (r

195 mediate (Sv(O(2)) target, 75-80%), and high (Sv(O(2)) target, >80%) ECMO blood flows were applied for

196 sed ECMO blood flow rate resulting in higher Sv(O(2)) decreases pulmonary artery pressure, cardiac ou

197 olar formation, as indicated by increases in Sv and TVvr.

198 Interestingly, Sv was not altered in group P but was significantly elev

199 Low (Sv(O(2)) target, 70-75%), intermediate (Sv(O(2)) target, 75-80%), and high (Sv(O(2)) target, >80

200 Methods: Low (Sv(O(2)) target, 70-75%), intermediate (Sv(O(2)) target,

201 LT/Sv oocytes also arrest at metaphase of meiosis I, rather

202 BALB/c and C58 (the progenitor strains of LT/Sv) and crosses of these two progenitor strains and foun

203 se I arrest was investigated using strain LT/Sv and LT-related recombinant inbred strains, LTXBO and

204 Strain LT/Sv female mice show a high frequency of spontaneous ovar

205 Strain LT/Sv mice, and strains related to LT/Sv, produce a high pe

206 that these traits are polygenic and that LT/Sv mice inherited a novel combination of permissive alle

207 Strain LT/Sv mice, and strains related to LT/Sv, produce a high percentage of atypical oocytes that a

208 e physiologic effects of different levels of Sv(O(2)) obtained by changing ECMO blood flow in patient

209 were established on both a mixed 129 OlaHsd/Sv and C57BL/6 background and a pure 129 OlaHsd/Sv backg

210 and C57BL/6 background and a pure 129 OlaHsd/Sv background.

211 ment in AUC was statistically significant on Sv with p-values of 0.032 and 0.04 compared to using onl

212 rd test was performed (thermodilution and/or Sv o2 ) were included.

213 flow rate affects mixed venous oxygenation (Sv(O(2))) during venovenous extracorporeal membrane oxyg

214 An excess relative risk estimate of 10.5 per Sv (10 cases) was observed for kidney cancer; this may h

215 ut also preferentially exposes more in-plane Sv while limiting edge Sv exposure, which is conducive t

216 oderate reliability for Scv o2 in predicting Sv o2 in critical care patients with variability based o

217 The ICC for reference Sv o2 was 0.83 (95% CI, 0.75-0.89) with a mean differenc

218 n estimating mixed venous oxygen saturation (Sv o2 ) and cardiac index in critically ill patients.

219 put (Q), and mixed venous oxygen saturation (Sv(O(2))) were measured by flotation catheter.

220 .85, 0.79 and 0.89 on independent test set ( Sv , N = 47) using Ffd , Ft , and their combination, res

221 gnated by a special named unit, the sievert (Sv).

222 etermined in rough (Rv) and isogenic smooth (Sv) variants of A. actinomycetemcomitans cultured in hal

223 pressed in the zebrafish ventral subpallium (Sv, septum), and in the supra-/postcommissurally lying p

224 e discharges to be as high as 0.13 sverdrup (Sv) (1 Sv = 1 million cubic meters per second) during He

225 ntegrated value of up to 30 to 40 sverdrups (Sv) (1 Sv = 10(6) cubic meters per second), and it occur

226 erage overturning is 18.7 +/- 5.6 sverdrups (Sv) (range: 4.0 to 34.9 Sv, where 1 Sv = a flow of ocean

227 tly upregulated in the Rv compared to in the Sv.

228 nalyzed 16 studies (1335 patients) that used Sv o2 as a reference and three studies (166 patients) th

229 not only promotes strain and sulfur vacancy (Sv) generation but also preferentially exposes more in-p

230 usion protein transgenic mice (C57BL/6NTac x Sv/129), and CD40L-deficient mice with spontaneous Pneum