ライフサイエンスコーパス: VAC

1 VAC and VAI or VIE with surgery (with or without RT), ar

2 VAC events were associated with significantly increased

3 VAC is an objective measure which can be readily obtaine

4 VAC is defined by increases in fraction of inspired oxyg

5 VAC is demonstrated here to occur early in frontotempora

6 VAC may be a useful surveillance tool.

7 VAC signals were most often caused by volume overload an

8 VAC, like other poxviruses, has a linear, double-strande

9 VAC-treated wounds were characterized by the formation o

10 in (2.9 +/- 2.0 vs. 1.6 +/- 2.8; p < 0.002), VAC (-0.21 +/- 0.17 vs. -0.09 +/- 0.15; p < 0.0001), and

11 .5 mg/m(2), and cyclophosphamide 2.2 g/m(2) (VAC) and vincristine 1.5 mg/m(2), topotecan 0.75 mg/m(2)

12 parahydrogen gas supply and a single 110/220 VAC power source.

13 Allocated treatment was either 7 VAC courses with 1.5 g/m(2) of cyclophosphamide or seven

14 We found that disrupting a VAC-localized cysteine protease compromised VAC digestiv

15 Gene regulatory analysis identifies a VAC-specific network and the Populus MYB48 as its primar

16 he barriers to genetic testing for VM across VACs, described differences between VACs based on size,

17 factor for development of hepatopathy after VAC therapy was age.

18 ver, response interventions for both IPV and VAC are rare and predominantly implemented in high-incom

19 rventions that prevent or respond to IPV and VAC by parents or caregivers, aiming to identify common

20 Key mechanisms for reducing IPV and VAC in primary prevention interventions included improve

21 eness of the adverse consequences of IPV and VAC on children.

22 nce in support of efforts to address IPV and VAC through coordinated prevention and response programm

23 he use of health services to address IPV and VAC together.

24 e identified, with 20 targeting both IPV and VAC.

25 sing both prevention and response to IPV and VAC.

26 chanisms that lead to a reduction in IPV and VAC.

27 ied by derangements of contractile state and VAC.

28 g selected sequences from MPXV, variola, and VAC-V in MPXV-infected individuals than MVA vaccinees.

29 ide (VAC) or vincristine, melphalan (VM) and VAC.

30 ducation were barriers to genetic testing at VACs of all sizes.

31 ear correlation (r = 0.82, P < .001) between VAC derived from cardiac MRI and from PV loop data.

32 We analyzed the association between VAC and clinical diagnoses, ICU length of stay, duration

33 tudies, we evaluated 35 associations between VAC and adverse health outcomes, identifying 27 statisti

34 ide pools that are highly homologous between VAC-V and MPXV 2022, with the highest frequency of respo

35 M across VACs, described differences between VACs based on size, and proposed multiple interventions

36 ur strategy to construct a nearly 200,000-bp VAC-bacterial artificial chromosome (BAC) was based on c

37 sion along with mechanical forces exerted by VAC therapy was associated with the formation of more ph

38 intracellular acidic compartments per cell (VAC), and we show here that inhibition of the increase i

39 d types, we uncover vessel-associated cells (VAC), a largely uncharacterized parenchyma subtype and t

40 terminate in the ventral association center (VAC).

41 p, representing 81 vascular anomaly centers (VACs) serving individuals up to 18 years of age, to comp

42 roimaging data were analyzed to characterize VAC-FTD and compare VAC-FTD with control groups.

43 iolence (IPV) and violence against children (VAC) are still disparate worldwide, despite increasing e

44 d maltreatment or violence against children (VAC) has not yet been comprehensively evaluated.

45 mechanisms by which vacuum assisted closure (VAC) modulates wound angiogenesis are still largely unkn

46 livered through the Vacuum Assisted Closure (VAC) Therapy System.

47 analyzed to characterize VAC-FTD and compare VAC-FTD with control groups.

48 d resembled the vacuolar apical compartment (VAC) previously observed in epithelial cells that lose c

49 n intracellular vacuolar apical compartment (VAC) when prevented from polarizing.

50 ogenesis of the virion assembly compartment (VAC), increased secretion of noninfectious particles, an

51 ies a newly recognized vacuolar compartment (VAC) that undergoes dynamic fragmentation during T. gond

52 -like vacuole (PLV) or vacuolar compartment (VAC).

53 in the total volume of acidic compartments (VAC), mainly constituted by lysosomes, is a common event

54 Ventilator-associated complications (VAC) is a simple, objective measure of respiratory deter

55 VAC-localized cysteine protease compromised VAC digestive function and markedly reduced chronic infe

56 definition, ventilator-associated condition (VAC), identifies patients with a period of sustained res

57 n-related) ventilator-associated conditions (VAC, IVAC) and VAP.

58 underwent the Variable Attentional Control (VAC) task.

59 ctile reserve, ventriculo-arterial coupling (VAC) reserve, and chronotropic response to the progressi

60 Ventriculo-arterial coupling (VAC) was derived from PV loop and cardiac MRI data.

61 COVI-VAC inoculation generated spike IgG antibody levels and

62 COVI-VAC was developed by recoding a segment of the viral spi

63 COVI-VAC was temperature sensitive in vitro yet grew robustly

64 Highly attenuated COVI-VAC is protective at a single intranasal dose in a relev

65 Here, we describe COVI-VAC, the only live attenuated severe acute respiratory s

66 r the furin cleavage site deletion, the COVI-VAC and parental SARS-CoV-2 amino acid sequences are ide

67 Upon challenge with WT virus, COVI-VAC vaccination reduced lung challenge viral titers, res

68 s auratus) vaccinated intranasally with COVI-VAC compared to those inoculated with wild-type (WT) vir

69 The predictive value of COVID-VAC was demonstrated.

70 accination and the predictive value of COVID-VAC, a novel scale, among adults in the four largest US

71 al substrates of visual artistic creativity (VAC) are unknown.

72 and emergence of visual artistic creativity (VAC-FTD) were matched to 2 control groups based on demog

73 ication, vibration assisted crystallization (VAC) that produces superior films, which approach the fu

74 cristine, dactinomycin and cyclophosphamide (VAC) during weeks 6 to 41 (VTC/VAC).

75 ristine, dactinomycin, and cyclophosphamide (VAC) or vincristine, melphalan (VM) and VAC.

76 and dactinomycin (VA) and cyclophosphamide (VAC, n = 235), or VA and ifosfamide (VAI, n = 222), or v

77 incristine, topotecan, and cyclophosphamide (VAC/VTC).

78 ristine, dactinomycin, and cyclophosphamide (VAC; total cumulative cyclophosphamide dose, 26.4 g/m(2)

79 vincristine, dactinomycin, cyclophosphamide (VAC), and XRT did not significantly improve survival in

80 ristine, dactinomycin, and cyclophosphamide [VAC] v vincristine, dactinomycin, and ifosfamide [VAI])

81 % +/- 1.4, P = .007) and cardiac MRI-derived VAC (-0.6 +/- 0.6 vs 0.3 +/- 0.3, P = .001) significantl

82 (r = 0.67, P = .005) and cardiac MRI-derived VAC (r = 0.60, P = .01).

83 (r = 0.60, P = .01), and cardiac MRI-derived VAC (r = 0.61, P = .01) had a significant linear relatio

84 microbial genera (genes) that distinguished VAC, CHE and CLE from UNF, CHE from CLE, and CHE from VA

85 rated according to correct responses in each VAC load.

86 ial were randomly assigned to receive either VAC alone or VAC alternating with vincristine, topotecan

87 The engineered VAC genomes can then be used to produce clonally pure re

88 icial chromosome (BAC) containing the entire VAC genome can be engineered in Escherichia coli by homo

89 Stable plasmids containing the entire VAC genome, with an intact concatemer junction sequence,

90 e 3.9 (95% confidence interval, 2.9-5.3) for VAC, 2.5 (1.5-4.1) for IVAC, 2.0 (1.1-3.6) for VAE-VAP,

91 is highlights substantial health impacts for VAC survivors, underscoring the need for health system p

92 and CLE from UNF, CHE from CLE, and CHE from VAC, respectively.

93 occipital region was strongly correlated in VAC-FTD, but not in NVA-FTD or HC, with a volume in the

94 or the inhibition of TNF-induced increase in VAC and cell death.

95 show here that inhibition of the increase in VAC due to PMCA4 deficiency not only reduced cell death

96 by inhibition of the TNF-induced increase in VAC.

97 in wild-type L929 cells, while increases in VAC due to genetic mutation, senescence, cell culture co

98 hin the patient-specific atrophy patterns in VAC-FTD (17 of 17) and NVA-FTD (45 of 51 [88.2%]).

99 Rescue of infectious VAC was consistently achieved by transfecting the VAC-BA

100 Patients received intravenous VAC/VI chemotherapy with a cyclophosphamide dose of 1.2

101 alternating with vincristine and irinotecan (VAC/VI) combined with temsirolimus followed by maintenan

102 n performances of high, intermediate and low VAC load FC on HC-SCZ and HC-SIB cohorts were tested thr

103 M-VAC remains the standard of care for metastatic transiti

104 M-VAC was recycled every 21 days, with prophylactic recomb

105 treatment was five cycles of chemotherapy (M-VAC: methotrexate, vinblastine, doxorubicin, and cisplat

106 te, vincristine, adriamycin and cisplatin (M-VAC) chemotherapy has been the standard of therapy for o

107 , vinblastine, doxorubicin, and cisplatin (M-VAC) chemotherapy to assess an impact on long-term survi

108 , vinblastine, doxorubicin, and cisplatin (M-VAC) was performed in poor-risk patients with advanced u

109 , vinblastine, doxorubicin, and cisplatin (M-VAC) was superior to single-agent cisplatin in patients

110 , vinblastine, doxorubicin, and cisplatin (M-VAC), the standard chemotherapy regimen for locally adva

111 are unlikely to benefit significantly from M-VAC chemotherapy.

112 Assessment of dose-intense M-VAC as salvage treatment in patients who failed to respo

113 Dose-intense M-VAC is superior to gallium nitrate/5-FU in poor-risk pat

114 Dose-intense M-VAC was associated with a greater incidence of neutropen

115 receive either two courses of neoadjuvant M-VAC followed by surgery plus three additional cycles of

116 TCC, previously reported in five trials of M-VAC chemotherapy.

117 y assigned to treatment with either FAP or M-VAC.

118 tion of the intergroup trial confirms that M-VAC is superior to single-agent cisplatin in patients wi

119 term follow-up evaluation, survival in the M-VAC arm continues to be superior to cisplatin (P = .0001

120 d 5-FU arm was 19 versus 17 months for the M-VAC arm, with a median follow-up duration of 35 months (

121 e FAP arm and more myelosuppression in the M-VAC arm.

122 Thus, FAP is very likely to be inferior to M-VAC and is certainly no less toxic.

123 Only 3.7% of the patients randomized to M-VAC are alive and continuously disease-free at 6 years.

124 lium nitrate/5-FU combination responded to M-VAC as second-line therapy (42%; 95% CI, 15.2% to 72.3%)

125 nificantly different, patients assigned to M-VAC had a much better chance of responding to front-line

126 Among the patients assigned to M-VAC, 51 (59%) of 86 had an objective response, with comp

127 Sixteen of 17 patients treated with M-VAC (94%; 95% CI, 71.3% to 99.8%) demonstrated a major r

128 ate, the median survival for patients with M-VAC remained unsatisfactory.

129 Of 689 patients with FTD, 17 (2.5%) met VAC-FTD inclusion criteria (mean [SD] age, 65 [9.7] year

130 Moreover, VAC-treated wounds displayed a well-oxygenated wound bed

131 rcularization of head-to-tail concatemers of VAC DNA.

132 All cases occurred after cycles of VAC (n = 16) or vincristine and cyclophosphamide with co

133 Therapy included four cycles of VAC followed by four cycles of VA over 22 weeks.

134 There was no difference in effect of VAC versus VAC/VTC across risk groups.

135 t the mechanisms underlying the emergence of VAC in FTD.

136 Emergence of VAC occurred around the time of onset of symptoms and wa

137 predispose some patients to the emergence of VAC under certain environmental or genetic conditions.

138 continued efforts to eliminate all forms of VAC.

139 Incidences of VAC, IVAC, VAE-VAP, and VAP according to prospective sur

140 bition of lysosome exocytosis or increase of VAC by sucrose restored the sensitivity of PMCA(mut) cel

141 sis is also associated with the increases of VAC.

142 ncertainty surrounding the noninferiority of VAC compared with VAI remains at this stage.

143 events in the promoter and coding region of VAC-INVcis-QTL were also detected for ADP-glucose pyroph

144 The discovery of MYB48 as a key regulator of VAC function highlights a previously uncharacterized mec

145 The utility of VAC prevention bundles merits assessment.

146 ological analyses revealed that formation of VACs and endocytosis of TJ proteins was mediated by Rho-

147 The IFN-gamma dependent formation of VACs required ATPase activity of a myosin II motor but w

148 K-mediated, myosin II-dependent formation of VACs.

149 essel number and size, pointing to a role of VACs in vessel development.

150 r progressive disease after TC received only VAC.

151 omly assigned to receive either VAC alone or VAC alternating with vincristine, topotecan, and cycloph

152 somal organelle (the vacuolar compartment or VAC) in turnover of autophagosomes and persistence durin

153 rofiles for patients who received VTC/VAC or VAC alone were comparable.

154 Vacuum packaging (VAC), modified atmosphere packaging (MAP) and dry-ageing

155 ruary 2000 and March 2010 (n = 431 receiving VAC and n = 425 receiving VAI).

156 modifications for younger children receiving VAC therapy are recommended.

157 Cells were infected with a recombinant VAC containing inserted sequences for plasmid replicatio

158 vations that chemical inhibitors that reduce VAC also reduced the plasma membrane disruption induced

159 For intermediate-risk RMS, VAC/VTC does not significantly improve FFS compared with

160 ng was more common at large and medium-sized VACs.

161 Small VACs were more likely to use oncology-based platforms, w

162 rhabdomyosarcoma (RMS) treated with standard VAC (vincristine, dactinomycin, and cyclophosphamide) ch

163 of Toxoplasma persistence and suggests that VAC proteolysis is a prospective target for pharmacologi

164 NPWT delivered by the VAC Therapy System seems to be a safe and effective trea

165 ions were significantly less frequent in the VAC arm (< 1%) than in the VAI arm (7%), mainly resultin

166 ienced more frequent thrombocytopenia in the VAC arm (45% v 35%) but fewer grade 2 to 4 acute tubular

167 two groups (64.8% [95% CI 55.5-74.1] in the VAC/VI group vs 66.8% [57.5-76.2] in the VAC/VI plus tem

168 62 events in 60 [41%] of 148 patients in the VAC/VI group vs 89 events in 87 [58%] of 149 patients in

169 ) of 148 patients were FOXO1 negative in the VAC/VI group, and 108 (73%) of 149 were FOXO1 negative i

170 the VAC/VI group vs 66.8% [57.5-76.2] in the VAC/VI plus temsirolimus group (hazard ratio 0.86 [95% C

171 89 events in 87 [58%] of 149 patients in the VAC/VI with temsirolimus group), lymphopenia (83 events

172 There was one treatment-related death in the VAC/VI with temsirolimus group, categorised as not other

173 108 (73%) of 149 were FOXO1 negative in the VAC/VI with temsirolimus group.

174 Death of parasites lacking the VAC protease was preceded by accumulation of undigested

175 ne secretion and facilitate formation of the VAC for efficient infectious virus production.

176 poxia limited to the direct proximity of the VAC-foam interface, where higher VEGF levels were found.

177 Logistics and barriers varied by size of the VAC.

178 Results were stratified by size of the VAC.

179 ganization into structures that resemble the VAC and a decrease in cytokine release.

180 as consistently achieved by transfecting the VAC-BAC plasmids into mammalian cells that were infected

181 We also provide evidence that within the VAC or late endosome this protease mediates the proteoly

182 uminal compartment that is distinct from the VACs of MDCK cells.

183 264 were randomly assigned to VAC and 252 to VAC/VTC; 101 PME patients were nonrandomly treated with

184 nto the study: 264 were randomly assigned to VAC and 252 to VAC/VTC; 101 PME patients were nonrandoml

185 In 297 evaluable patients (148 assigned to VAC/VI alone and 149 assigned to VAC/VI with temsirolimu

186 assigned to VAC/VI alone and 149 assigned to VAC/VI with temsirolimus), the median age was 6.3 years

187 fit was apparent from the addition of DOX to VAC chemotherapy in patients with gross residual EOE.

188 25 [49%] female) groups were well matched to VAC-FTD demographically.

189 Addition of temsirolimus to VAC/VI did not improve event-free survival in patients w

190 r luminal compartment in Par1b-MDCK cells to VACs characteristic of control MDCK cells, indicating a

191 of animals (UNF: unvaccinated, unchallenged; VAC: vaccinated, challenged; CHE: unvaccinated, challeng

192 gusto (STA), Sao Gabriel (SAG), and Vacaria (VAC).

193 ty against MPXV and vaccinia-based vaccines (VAC-V), but studies are limited.

194 limus followed by maintenance therapy versus VAC/VI alone with maintenance therapy.

195 re was no difference in effect of VAC versus VAC/VTC across risk groups.

196 The large capacity of vaccinia virus (VAC) for added DNA, cytoplasmic expression and broad hos

197 he ability to manipulate the vaccinia virus (VAC) genome, as a plasmid in bacteria, would greatly fac

198 ophosphamide (VAC) during weeks 6 to 41 (VTC/VAC).

199 icity profiles for patients who received VTC/VAC or VAC alone were comparable.

200 rs, 4-year FFS was 73% with VAC and 68% with VAC/VTC (P = .3).

201 low-up of 4.3 years, 4-year FFS was 73% with VAC and 68% with VAC/VTC (P = .3).

202 increase in 5-year FFS from 64% to 75% with VAC/VTC.

203 not significantly improve FFS compared with VAC.

204 lication (IVAC), requires that patients with VAC also have an abnormal temperature or white blood cel

205 We assessed 153 patients with VAC and 390 without VAC.

206 ion and nonoverlapping toxicity profile with VAC makes this combination an attractive candidate for f

207 Three-year FFS rates with VAC, VAI, and VIE were 75%, 77%, and 77%, respectively (

208 topotecan received continuation therapy with VAC alone.

209 Nonresponders were treated with VAC alone.

210 hemotherapy to that of patients treated with VAC alternating with vincristine, topotecan, and cycloph

211 tracranial extension (PME) were treated with VAC and immediate x-ray therapy.

212 mpared with that of 24 patients treated with VAC and XRT without DOX (65% alive at 10 years, P = .93)

213 1 PME patients were nonrandomly treated with VAC.

214 ed myosin II was observed to colocalize with VACs after IFN-gamma exposure.

215 sessed 153 patients with VAC and 390 without VAC.