ライフサイエンスコーパス: culprit

1 hat the KCNE2 variant was not the underlying culprit.

2 ta oligomers are thought to be a major toxic culprit.

3 spindle attachment in meiosis as a potential culprit.

4 cation channel activity as a likely link and culprit.

5 r chromosome pairing and synapsis may be the culprit.

6 mplicate levamisole-adulterated cocaine as a culprit.

7 kinin and its metabolites is thought to be a culprit.

8 showing that molecular oxygen itself is the culprit.

9 ulfate-reducing bacteria (SRB) are the major culprit.

10 iatric population with new drugs included as culprit.

11 gevity of dentin bonding is one of the major culprits.

12 d function have been identified as potential culprits.

13 eaflet adaptation are considered mechanistic culprits.

14 ades but with few consensuses for the likely culprits.

15 dium are deranged and what is the underlying culprit?

16 culprit 1.66 [IQR 1.40-2.25] vs highest non-culprit 1.24 [1.06-1.38], p<0.0001).

17 (median maximum tissue-to-background ratio: culprit 1.66 [IQR 1.40-2.25] vs highest non-culprit 1.24

18 d in 20 patients with acute stroke (21 [27%] culprit, 12 [15%] probably culprit, and 45 [58%] nonculp

19 and nonculprit vessel (STEMI, 1.7 versus SA culprit, 2.8; P</=0.001 and SA nonculprit, 2.9; P<0.0001

20 Surprisingly, it was found that the main culprits affecting the yield and enantioselectivity were

21 n provocation test is needed to identify the culprit allergen or allergens.

22 Medical history was assessed, and culprit allergen source and anaphylaxis severity grade w

23 ost potent trigger of this syndrome, but the culprit allergens have not yet been identified.

24 Culprit allergens responsible include house dust mite, g

25 Thus, alpha345NC1 hexamers are the culprit alloantigen and primary target of all alloantibo

26 s irrespective of whether AX or Clav was the culprit, although differences in cytokine secretion were

27 ncy of left main or left anterior descending culprit and cardiogenic shock than STEMI-ATH.

28 ide or (18)F-fluorodeoxyglucose can identify culprit and high-risk carotid plaque.

29 18)F-fluoride tissue-to-background ratios of culprit and non-culprit coronary plaques of patients wit

30 scernible, there were no differences between culprit and non-culprit plaques (1.71 [1.40-2.13] vs 1.5

31 play a role in plaque vulnerability of both culprit and nonculprit coronary vessels.

32 ompared with the stable angina patients both culprit and nonculprit vessel (STEMI, 1.7 versus SA culp

33 microcirculation (stable angina [SA] cohort: culprit and nonculprit vessel) and acute microcirculator

34 (18)F-Fluoride PET/CT highlights culprit and phenotypically high-risk carotid plaque.

35 t crops, therefore, are clearly not the only culprit and, likely, not even the primary culprit: Not o

36 brillar soluble oligomers are the neurotoxic culprits and are associated with the pathology of AD.

37 stroke (21 [27%] culprit, 12 [15%] probably culprit, and 45 [58%] nonculprit plaques).

38 e immunosuppressive therapy, the most likely culprits are primary lung cancer, chronic infectious or

39 ington's disease (HD); however, the cellular culprits are unclear.

40 and extracellular changes in response to the culprit arrhythmia have been identified, but specific pa

41 cognition of AIC and prompt treatment of the culprit arrhythmia using pharmacological or ablative tec

42 Therapeutic choice depends on the culprit arrhythmia, patient comorbidities, and preferenc

43 However, whole vessel TBR(max) was higher in culprit arteries for FDG (1.92 [0.41] versus 1.71 [0.31]

44 hether early detection of occluded potential culprit arteries leads to interventions that improve out

45 in Myocardial Infarction flow 0 or 1 in the culprit artery (P=0.020), incomplete ST-segment resoluti

46 a coronary flow reserve (CFR</=2.0), in the culprit artery after emergency percutaneous coronary int

47 ol took place after revascularization of the culprit artery and comprised 3 phases: first, epicardial

48 IMR and CFR were measured in the culprit artery at the end of percutaneous coronary inter

49 ogenic shock, early revascularization of the culprit artery by means of percutaneous coronary interve

50 HMR in the culprit artery in patients with MVI was significantly hi

51 localized in the perfusion territory of the culprit artery in the absence of necrosis, although the

52 In STEMI-SCAD, the culprit artery was more commonly left main (13% vs. 1%)

53 y performed soon after recanalization of the culprit artery, cardiac magnetic resonance performed dur

54 In the decision between culprit artery-only and multivessel percutaneous coronar

55 w after ischaemia, despite re-opening of the culprit artery.

56 29% +/- 8) in the perfusion territory of the culprit artery.

57 ery responsible for the infarct (infarct, or culprit, artery) improves prognosis.

58 a consensus report entitled Identifying the Culprit: Assessing Eyewitness Identification In this rev

59 Here, we briefly discuss all drug culprits associated with ANCA vasculitis and then focus

60 The presence of activated neutrophils in culprit atherosclerotic plaques of patients with unstabl

61 It is essential to determine the possible culprit because this will improve secondary stroke preve

62 As the culprit behind most cancer-related deaths, metastasis is

63 esvirus (KSHV) is an oncogenic virus and the culprit behind the human disease Kaposi sarcoma (KS), an

64 e Arg(838) substitutions in RetGC1 being the culprit behind the pathogenesis of the CORD6 congenital

65 dentify chemotherapy-induced senescence as a culprit behind tumor promotion, suggesting that eliminat

66 A 7-day challenge with the culprit beta-lactam may yield more positive reactions th

67 lerotic coronary vasculature is not only the culprit but also a victim of myocardial ischemia/reperfu

68 diovascular toxicities were suspected as the culprit but not directly assessed in the study.

69 arotid endarterectomy and 8 controls without culprit carotid atheroma.

70 rate increased uptake of both FDG and NaF in culprit carotid plaques, with discrete distributions of

71 k or minor ischemic stroke: 18 patients with culprit carotid stenosis awaiting carotid endarterectomy

72 pathogenic proteins, considering them as the culprits causing neuronal damage and degeneration.

73 e phenotypes makes identification of genetic culprits challenging.

74 ory diseases, including atherosclerosis, the culprit condition of myocardial infarction and stroke.

75 onset and who had complete occlusion of the culprit coronary artery to receive a bolus injection of

76 onary angiography having an acutely occluded culprit coronary artery.

77 ssue-to-background ratios of culprit and non-culprit coronary plaques of patients with acute myocardi

78 ofen in all cases, and additionally with the culprit drug (if different) in those patients that toler

79 -13 and IL-5 was detected in presence of the culprit drug compared with the alternative drug.

80 f selective COX-2 inhibitors can replace the culprit drug if the chronic treatment is necessary, alth

81 ert future reactions and should identify the culprit drug or drugs and safe alternatives.

82 nsitivity (NSAIDH), challenge tests with the culprit drug yield negative results.

83 t should at least contain information on the culprit drug(s) including international nonproprietary n

84 drugs whereas BAT was applied only with the culprit drug.

85 reaction and those that help to identify the culprit drug.

86 s were also subsequently challenged with the culprit drug.

87 e patients (30-56% of patients, depending on culprit-drug).

88 The culprit drugs include commonly used medications includin

89 not develop hypersensitivity when exposed to culprit drugs suggesting a nonlinear, multifactorial rel

90 e NSAIDs were directly challenged with their culprit drugs.

91 (64)Cu-FBP8 PET to detect source thrombi and culprit emboli after deep vein thrombosis and pulmonary

92 actor closely tied to temperature may be the culprit exposure.

93 d analyze the possibility of introducing the culprit fish or other nonrelated fish to avoid unnecessa

94 In 99% of cases culprit food allergens were plant-derived, mainly vegeta

95 (Abeta) peptide, accumulation of which is a culprit for Alzheimer's disease (AD), is derived from th

96 tive pathogen of Chagas disease and the main culprit for cardiac-related mortality in Latin-America t

97 ndicating that neurodegeneration is the main culprit for cases of mild FD.

98 defenses following influenza as the primary culprit for enhanced susceptibility to secondary bacteri

99 HIV-1 Tat is a major culprit for HIV/neuroAIDS.

100 We found that a major culprit for mitotic slippage involves reduction of MAD2

101 ocytes in individuals with ASD as a possible culprit for neural defects, we were able to increase syn

102 lifestyle represents a convenient catch-all culprit for such exposures, effective treatment and prev

103 An obvious culprit for the discrepancy is the use of dozens of diff

104 The main culprit for the dramatic shortfall in the performance of

105 of amyloid-beta peptide (Abeta) as the main culprit for the myriad physiological changes seen during

106 nce of tumor-initiating cells (T-ICs) as the culprit for treatment resistance.

107 Bacterial pathogens are the main culprits for outbreaks of food-borne illnesses.

108 han residential real estate assets are major culprits for the failure of over 350 US commercial banks

109 [(18)F]FDG mTBRmax differentiated culprit from nonculprit carotid lesions (median differen

110 t for muscular dystrophies by correcting the culprit genomic mutations and enabling normal expression

111 Legal drug culprits have been implicated as causative agents in sec

112 n sequencing of 560 genes, including genetic culprits implicated in AF, the Mendelian cardiomyopathie

113 atus, which in turn is proposed as a primary culprit in AD pathogenesis.

114 eta) peptide is a major underlying molecular culprit in Alzheimer disease.

115 ies, have long been conceived as the primary culprit in delinquent behavior.

116 etion, rather than sodium deficiency, is the culprit in dilutional hyponatremia, isotonic saline admi

117 he fetus and that T cell activation may be a culprit in postsurgical pregnancy complications.

118 Host mediated damage is also a culprit in pulmonary injury as both innate and adaptive

119 tissue expansion and shape and suggested as culprit in several congenital diseases such as CAKUT (Co

120 Although clonal mast cell disease is the culprit in some individuals, it does not fully explain t

121 One culprit in sustained inflammation is the activated infla

122 d oxidation (FAO) has long been considered a culprit in the development of obesity/diabetes mellitus-

123 r complete ETT occlusion was noted to be the culprit in the majority of these patients.

124 2O2) causes oxidative stress and is the main culprit in the pathogenesis of ischemia/reperfusion (I/R

125 failure of pancreatic beta-cells is the main culprit in the pathophysiology of diabetes, a disease th

126 llogenic pathway and are putative pathogenic culprits in Alzheimer's disease (AD).

127 Anthracycline compounds are major culprits in chemotherapy-induced cardiotoxicity, which i

128 ions of erroneous DSB repair and are crucial culprits in malignant transformation and IR-induced cell

129 (TLRs) have long been considered to be major culprits in the development of atherosclerosis, contribu

130 ble by conventional microscopy, as potential culprits in the pathogenesis of neurodegenerative diseas

131 lular alpha-synuclein fibers that are likely culprits in the spread of Parkinson's disease.

132 nib, as well as antiviral agents, suppressed culprit-induced T cell proliferation in vitro, further s

133 uited to inflammatory sites are the cellular culprits inducing thrombocytopenic tissue hemorrhage.

134 BAT seems to add more information about the culprit insect even if the true clinical relevance of BA

135 ) and details related to the sting reaction (culprit insect, localization of the sting, time interval

136 ion to HBV and YJV that did not identify the culprit insect.

137 Among the culprits involved in these illnesses are prions and prio

138 Identification of the specific seed as the culprit is often not explored or is difficult to verify.

139 cipants as follows: class 1, plaque-mediated culprit lesion (82.5% of women; 94.9% of men); class 2,

140 on model for the presence of an angiographic culprit lesion and internally validated with bootstrappi

141 al stent implantation characteristics at the culprit lesion and residual intrastent plaque/thrombus p

142 omplications associated with stenting of the culprit lesion following ACS.

143 ocardiographic changes or an atherosclerotic culprit lesion identified during angiography.

144 ges indicating myocardial ischemia, an acute culprit lesion may be present and patients may benefit f

145 ssed the prognostic impact of postprocedural culprit lesion OCT findings in patients with acute coron

146 rction and Multivessel Disease: Treatment of Culprit Lesion Only or Complete Revascularization), we r

147 In the CULPRIT-SHOCK trial (The Culprit Lesion Only PCI Versus Multivessel PCI in Cardio

148 In a subanalysis of the CULPRIT-SHOCK trial (Culprit Lesion Only PCI versus Multivessel PCI in Cardio

149 The CULPRIT-SHOCK trial (Culprit Lesion Only PCI Versus Multivessel PCI in Cardio

150 up for intended nonculprit lesion PCI versus culprit lesion only PCI.

151 ong those who initially underwent PCI of the culprit lesion only than among those who underwent immed

152 ascularization strategies: either PCI of the culprit lesion only, with the option of staged revascula

153 cutaneous coronary intervention (PCI) of the culprit lesion reduces the risk of cardiovascular death

154 Postprocedural OCT assessment of treated culprit lesion revealed at least one of these parameters

155 ymorphonuclear cells [PMNs]) accumulation in culprit lesion site (CLS) thrombus is a predictor of car

156 tistical evidence for effect modification by culprit lesion vessel (P=0.8).

157 A definite or possible culprit lesion was identified by OCT in 46.2% (67/145) o

158 Associations of the likelihood of being a culprit lesion with both plaque contrast enhancement and

159 erval [CI]: 1.09 to 1.93 for new vs. initial culprit lesion).

160 ion of moderate stenoses, designation of the culprit lesion, and prediction of benefit from revascula

161 ent percutaneous coronary intervention for a culprit lesion, followed by intracoronary multimodality

162 ed in 1,189 patients, and the 2-year rate of culprit lesion-related MACE was not significantly associ

163 red in 18.0% of patients, of which 8.3% were culprit lesion-related, 10.7% were nonculprit lesion-rel

164 ndings were confirmed in ACS explored at the culprit lesion.

165 ents with AIS and angiographic evidence of a culprit lesion.

166 logy may potentially refine treatment of the culprit lesion.

167 xhibit similar (multiple) plaques beyond the culprit lesion.

168 he epicardial coronary artery containing the culprit lesion.

169 inically relevant; the identification of the culprit lesion; or whether the plaque (or patient) is at

170 Where is the culprit lesion?

171 ith complete revascularization compared with culprit-lesion only PCI (HR: 0.77; 95% confidence interv

172 e benefit of complete revascularization over culprit-lesion only PCI was consistent irrespective of t

173 andomized to staged nonculprit-lesion PCI or culprit-lesion only PCI.

174 artery disease who had undergone successful culprit-lesion PCI to a strategy of either complete reva

175 Following culprit-lesion PCI, 4,041 patients with STEMI and multiv

176 admission time, patients had a benefit from culprit-lesion-only as compared to immediate multivessel

177 er percutaneous coronary intervention of the culprit-lesion-only or immediate multivessel percutaneou

178 as compared with 339 patients (16.7%) in the culprit-lesion-only PCI group (hazard ratio, 0.51; 95% C

179 with 213 of the 2025 patients (10.5%) in the culprit-lesion-only PCI group (hazard ratio, 0.74; 95% c

180 ed in 158 of the 344 patients (45.9%) in the culprit-lesion-only PCI group and in 189 of the 341 pati

181 The relative risk of death in the culprit-lesion-only PCI group as compared with the multi

182 , complete revascularization was superior to culprit-lesion-only PCI in reducing the risk of cardiova

183 oint occurred in 56% of women treated by the culprit-lesion-only strategy versus 42% men, whereas 55%

184 nic Shock) demonstrated superior outcome for culprit-lesion-only versus immediate multivessel percuta

185 s with AIS were less likely to have coronary culprit lesions (7 of 29 versus 23 of 29; P<0.001) or an

186 Coronary culprit lesions are significantly less frequent in AIS p

187 s in acute coronary syndrome, especially for culprit lesions arising from the left coronary artery.

188 e majority of acute coronary events, and the culprit lesions demonstrate distinct histopathologic fea

189 Culprit lesions identified by OCT were classified as def

190 (Thrombus Aspiration in Thrombus Containing Culprit Lesions in Non-ST-Elevation Myocardial Infarctio

191 ll by coronary segment, excluding those with culprit lesions in X-ray angiography.

192 ibe the pathological and imaging findings in culprit lesions of patients with acute coronary syndrome

193 Culprit lesions of patients, who have had an acute coron

194 e primary end point was presence of coronary culprit lesions on coronary angiograms as analyzed by in

195 Plaques were dissected, and the culprit lesions used for histology and the measurement o

196 mong those with left circumflex or left main culprit lesions was 1.25 (95% CI, 1.02-1.53), for right

197 , and also the degree of inflammation in the culprit lesions.

198 ng techniques might thus fail to detect such culprit lesions.

199 ites and subsequent coronary events from new culprit lesions.

200 ur results suggest that cone opsins are the 'culprit' linking 11-cis-retinal deficiency to cone degen

201 pid Core Burden Index (maxLCBI(4mm)) and non-culprit major adverse cardiovascular events (NC-MACE).

202 Most often, the culprit morphology is plaque rupture with exposure of hi

203 ng whole-exome sequencing, we identified the culprit mutation (cG742T) in the RAS guanyl-releasing pr

204 Here we show that an unlikely culprit, namely the 5'-untranslated region (5'-UTR) of a

205 However, attempts at targeting the main culprits, neurotoxic Abeta peptides, have thus far prove

206 tic lesion upstream from a stroke), probably culprit (not the most stenotic lesion upstream from a st

207 ly culprit and, likely, not even the primary culprit: Not only did monarch and milkweed declines begi

208 ick test and if negative challenged with the culprit NSAID.

209 nd (4) negative oral provocation test to the culprit NSAID.

210 bodies against beta(2)-glycoprotein I as the culprit of APS.

211 nal stage of cancer progression and the main culprit of cancer related mortality.

212 nal stage of cancer progression and the main culprit of cancer-related mortality.

213 However, which EP receptor is the culprit of COX-2/PGE2-mediated neuronal inflammation and

214 Myeloid cells are a major culprit of IBMIR.

215 an the land clearing effect, the often cited culprit of malaria in the region.

216 dentified epithelial-derived IL-1beta as the culprit of mucositis onset, inducing mucosal barrier bre

217 Myofibroblasts, the culprit of organ fibrosis, can originate from mesenchyma

218 (EC) and smooth muscle cells (SMC) is a key culprit of pathologic vascular remodeling.

219 rd-open to outward-open dynamics was not the culprit of the broadening.

220 oligomers are generally considered to be the culprit of these diseases, the methodology currently ava

221 Common culprits of altered wound healing mechanics, including a

222 One of the main culprits of Alzheimer's disease (AD) is the formation of

223 ted farmland was shown to be one of the main culprits of Balkan endemic nephropathy.

224 d here identify CD4(+) and CD8(+) T cells as culprits of checkpoint inhibitor-associated immune encep

225 identified endogenous aldehydes as possible culprits of DNA damage that may induce the phenotypes se

226 isting, donor-specific antibodies (DSAs) are culprits of hyperacute rejection.

227 inine and poly proline-arginine, as the main culprits of NMD inhibition.

228 randomized trials comparing complete versus culprit-only revascularization in patients with ST-segme

229 ve Approaches (ISCHEMIA) and Complete versus Culprit-Only Revascularization Strategies to Treat Multi

230 In the COMPLETE (Complete vs Culprit-only Revascularization to Treat Multi-vessel Dis

231 substudy of the COMPLETEs trial (Complete vs Culprit-Only Revascularization to Treat Multi-Vessel Dis

232 The COMPLETE (Complete vs Culprit-only Revascularization to Treat Multi-vessel Dis

233 or myocardial infarction when compared with culprit-only revascularization.

234 ence interval =0.31-0.57) when compared with culprit-only revascularization.

235 Propionibacterium acnes are the most common culprit organisms, and treatment most often consists of

236 ascular disease (CVD) mortality was the main culprit, outpacing and overshadowing the effects of all

237 st coronary (18)F-NaF uptake was seen in the culprit plaque (median maximum tissue-to-background rati

238 were no differences between culprit and non-culprit plaques (1.71 [1.40-2.13] vs 1.58 [1.28-2.01], p

239 e 2 contrast enhancement was associated with culprit plaques (odds ratio 34.6; 95% confidence interva

240 take was increased in clinically adjudicated culprit plaques compared with asymptomatic contralateral

241 Culprit plaques had a higher degree of contrast enhancem

242 athological observations have all shown that culprit plaques in acute myocardial infarction are sever

243 degree of angiographic luminal narrowing in culprit plaques months to years before myocardial infarc

244 e uptake appeared to be increased in 7 of 16 culprit plaques, but no overall differences in uptake we

245 on tests (OPTs) with the PPIs other than the culprit PPI that displayed negative results in skin test

246 hat the prevention of aggregate formation in culprit proteins could retard the progression of amyloid

247 ll biological feature: the deposition of the culprit proteins in inclusion bodies.

248 on were more likely to have shock, left main culprit, proximal dissection, and initial TIMI (Thrombol

249 nd if negative, DPT was carried out with the culprit RCM.

250 ic and mechanistic aspects of four main drug culprits receiving attention of late, namely hydralazine

251 s can help focus mapping and ablation on the culprit regions, even when MRI is precluded by the prese

252 culates are not necessarily the sole or main culprit responsible for all harmful effects of DE.

253 ates the decidual cells of the mother as the culprit responsible for increased placental expression o

254 ingle-fraction dose delivered to the area of culprit scar.

255 Enrolled patients underwent scanning of non-culprit segments using NIRS-intravascular ultrasound ima

256 Methods and Results In a subanalysis of the CULPRIT-SHOCK trial (Culprit Lesion Only PCI versus Mult

257 The CULPRIT-SHOCK trial (Culprit Lesion Only PCI Versus Mult

258 In the CULPRIT-SHOCK trial (The Culprit Lesion Only PCI Versus

259 We analyzed patients from the CULPRIT-SHOCK trial with respect to the time of hospital

260 Out of 686 patients randomized in the CULPRIT-SHOCK trial, 444 patients (64.7%) presented duri

261 PET and coronary CTA demonstrated increased culprit site (18)F-FDG uptake more commonly in patients

262 s, being these levels more pronounced at the culprit site of coronary artery occlusion.

263 We examined (18)F-FDG uptake at the culprit sites of acute myocardial infarction (AMI) after

264 and their possible relation with severity or culprit soy product.

265 Aedes and Culex mosquitoes are the main culprits, spreading infection when they bite.

266 nd-generation DES over BMS in large coronary culprit ST-segment elevated myocardial infarction lesion

267 -FDG PET and coronary CTA 1-6 d after PCS of culprit stenoses.

268 ant susceptibility factor for many diseases, culprit T cell epitopes presented by disease-associated

269 TBR(max) (interquartile range) was higher in culprit than in nonculprit atheroma for both FDG (2.08 [

270 h identified plaque was classified as either culprit (the only or most stenotic lesion upstream from

271 as well as the identity of the critical main culprit: the amyloid-forming protein (red boxes).

272 MMP-9 may serve as the biochemical culprit to target and develop a novel approach for the t

273 uptake values in the clinically adjudicated culprit to the contralateral asymptomatic artery, and as

274 Events were subcategorized as culprit (treated) lesion-related, nonculprit (untreated)

275 erall differences in uptake were observed in culprit versus contralateral plaques or control patients

276 -blood ratios (mTBRmax) correctly identified culprit versus nonculprit arteries in patients with acut

277 G) and (18)F-sodium fluoride (NaF) uptake in culprit versus nonculprit carotid atheroma, (2) spatial

278 reserve were measured before stenting in the culprit vessel and in an angiographically normal nonculp

279 e ST-segment-elevation myocardial infarction culprit vessel if there was unstented segment amenable t

280 Early coronary angiography revealed a culprit vessel in 47%, with a total of 14% of patients u

281 lesion revascularization in the index event culprit vessel in patients with MVO.

282 inical use of fractional flow reserve in the culprit vessel may be preserved in selected patents with

283 Age, culprit vessel size and flow, and the presence of heart

284 ssure and flow velocity were recorded in the culprit vessel using a dual sensor wire while central ao

285 a large absorbed dose (112 and 374 Gy), the culprit vessel was identified in 1 case.

286 aphic confirmation of ST, OCT imaging of the culprit vessel was performed with frequency domain OCT.

287 aneous coronary intervention (MV-PCI) versus culprit vessel-only PCI (CO-PCI) in patients with multiv

288 us coronary intervention (PCI) compared with culprit vessel-only primary PCI.

289 Angiography was used to determine culprit vessel.

290 Predictors of culprit-vessel first revascularization were anterior/lat

291 real-world analysis comparing a strategy of culprit-vessel intervention (CVI) versus multivessel int

292 Performing culprit-vessel primary percutaneous coronary interventio

293 lloon time was 4 to 6 minutes shorter with a culprit-vessel revascularization first strategy.

294 o the as-treated revascularization strategy: culprit-vessel revascularization first, contralateral an

295 condary end points included the incidence of culprit vessels with acute occlusion.

296 cute respiratory syndrome coronavirus-2, the culprit virus, is highly contagious and stable in the en

297 The extraordinary culprit was ice cream, which had a frequent/occasional/n

298 Neither solution addresses a primary culprit, which is the culture of null hypothesis signifi

299 ting therapeutics that aim to target disease culprits with phenotypic modulators capable of altering

300 ing mitochondrial abnormalities as potential culprits within both nerve and muscle cells.