ライフサイエンスコーパス: culprit

1 spindle attachment in meiosis as a potential culprit.

2 cation channel activity as a likely link and culprit.

3 r chromosome pairing and synapsis may be the culprit.

4 mplicate levamisole-adulterated cocaine as a culprit.

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

6 Adverse drug reactions are a frequent culprit.

7 n and clopidogrel) is considered as the main culprit.

8 hat the KCNE2 variant was not the underlying culprit.

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

10 ades but with few consensuses for the likely culprits.

11 suggesting that miRNAs might be the elusive culprits.

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

13 dium are deranged and what is the underlying culprit?

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

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

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

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

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

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

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

21 Culprit allergens responsible include house dust mite, g

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

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

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

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

26 Intracoronary OCT imaging was performed at culprit and non-culprit plaques in patients presenting w

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

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

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

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

31 was to assess morphology and composition of culprit and stable coronary lesions by multidetector com

32 genesis with a focus on beta-amyloid both as culprit and therapeutic target.

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

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

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

36 itary spherocytosis and color blindness, the culprits are single point mutations to cysteine.

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

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

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

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

41 ortion of patients will not have an occluded culprit artery at cardiac catheterization.

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

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

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

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

46 P level 40 vs. 24 pg/ml, p = 0.005), and the culprit artery was more often the LAD in patients with B

47 The combination of no culprit artery with negative cardiac biomarker results w

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

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

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

51 29% +/- 8) in the perfusion territory of the culprit artery.

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

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

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

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

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

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

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

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

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

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

62 arotid endarterectomy and 8 controls without culprit carotid atheroma.

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

64 Pinpointing culprit causal variants along signal peaks of genome-wid

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

66 e phenotypes makes identification of genetic culprits challenging.

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

68 ) without vs 4.6% (95% CI, 3.4%-5.8%) with a culprit coronary artery (P = .33).

69 onfidence interval [CI], 12.2%-16.0%) had no culprit coronary artery and 127 (9.5%; 95% CI, 8.0%-11.2

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

71 ients with suspected STEMI by 3 criteria: no culprit coronary artery, no significant coronary artery

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

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

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

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

76 s were also subsequently challenged with the culprit drug.

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

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

79 The culprit drugs include commonly used medications includin

80 e NSAIDs were directly challenged with their culprit drugs.

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

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

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

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

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

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

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

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

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

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

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

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

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

94 d PAHs have thus been considered to be major culprits for lung cancer.

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

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

97 ed in disordered protein regions, as primary culprits for the high misalignment-related error levels

98 Looking for possible culprits for these latter processes, we analyzed hedgeho

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

100 ort evidence that Heparanse 2 (HPSE2) is the culprit gene for the syndrome.

101 As such, HNF4alpha is a culprit gene product for a monogenic and dominantly inhe

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

103 e of CF infection and identify an overlooked culprit-high-persister mutants producing elevated levels

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

105 ly implicate hepatic insulin resistance as a culprit in accumulation of free fatty acids as triglycer

106 eta (Abeta) peptide is thought to be a major culprit in Alzheimer disease (AD), and its production an

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

108 tor, which has been previously proposed as a culprit in autoimmunity, plays a critical role in SE-tri

109 These data indicate N-APP is not the sole culprit in axonal degeneration in adult nerves.

110 ective insulin secretion emerges as the main culprit in both monogenic and polygenic diabetes, with e

111 The culprit in coal tar that induces cancer was finally isol

112 ls, and an altered myocilin level may be the culprit in conditions such as corticosteroid glaucoma.

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

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

115 dered water molecule was identified as a key culprit in orienting retinal in a nonconstructive manner

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

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

118 One culprit in sustained inflammation is the activated infla

119 ta suggest that superoxide accumulation is a culprit in the abnormal sensory processing in the spinal

120 e of the brain has been hypothesized to be a culprit in the pathogenesis of Alzheimer's disease.

121 2O2) causes oxidative stress and is the main culprit in the pathogenesis of ischemia/reperfusion (I/R

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

123 eding requirements and is considered a major culprit in the rapidly increasing rates of obesity in de

124 egration, and homeostatic plasticity and are culprits in aberrant neuronal activity in certain epilep

125 xic products of oxidative metabolism seen as culprits in aging, neurodegenerative disease, and ischem

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 scuss hyperglycemia versus hyperlipidemia as culprits in diabetes-accelerated atherosclerosis and car

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

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

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

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

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

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

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

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

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

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

139 The analysis focused on patients with a culprit lesion (n = 270) and patients without a culprit

140 prit lesion (n = 270) and patients without a culprit lesion (n = 76) but with acetylcholine provocati

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

142 atients with acute coronary syndrome without culprit lesion and proof of coronary spasm during 3 year

143 ACS patients without culprit lesion and proof of coronary spasm have an excel

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

145 Thirty of 270 patients with culprit lesion died due to a cardiac cause (11.1%) and 1

146 Patients with a culprit lesion had a higher mortality and more coronary

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

148 cending coronary artery (LAD) versus non-LAD culprit lesion location (median BNP level 40 vs. 24 pg/m

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

150 sus patients <65 years of age with regard to culprit lesion morphology in acute myocardial infarction

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

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

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

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

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

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

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

158 The culprit lesion was defined by reviewing each patient's a

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

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

161 2 overlapping phases: first, addressing the culprit lesion, and second, aiming at rapid "stabilizati

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

163 at approximately 50% of ACS patients without culprit lesion, in whom intracoronary acetylcholine prov

164 In patients without culprit lesion, there was no cardiac death or nonfatal m

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

166 he epicardial coronary artery containing the culprit lesion.

167 coronary syndrome (ACS) in patients without culprit lesion.

168 in whom coronary angiography does not show a culprit lesion.

169 ruptured plaques in arteries other than the culprit lesion.

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

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

172 logy may potentially refine treatment of the culprit lesion.

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

174 Where is the culprit lesion?

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

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

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

178 ly attributable to recurrence at the site of culprit lesions and to nonculprit lesions.

179 Coronary culprit lesions are significantly less frequent in AIS p

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

181 -year-old group (32% vs. 9%, p = 0.009), and culprit lesions contained more thrombus in this group (1

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

183 Noninvasive identification of culprit lesions has the potential to improve noninvasive

184 Events were adjudicated to be related to culprit lesions in 12.9% of patients and to nonculprit l

185 on morphology and plaque composition between culprit lesions in ACS and stable lesions in ACS or stab

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

187 Culprit lesions in patients with ACS (n = 14) had signif

188 aque was 71%, 92%, and 85%, respectively, in culprit lesions in patients with ACS and in stable lesio

189 Differences between culprit lesions in patients with ACS and stable lesions

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

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

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

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

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

195 c total occlusions, and those with uncertain culprit lesions were excluded.

196 e myocardial infarctions develop at sites of culprit lesions without a significant stenosis.

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

198 to be related to either originally treated (culprit) lesions or untreated (nonculprit) lesions.

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

200 principle that ADMA plays a causal role as a culprit molecule in atherosclerosis and support recent e

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

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

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

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

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

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

207 mulation, which has been suggested to be the culprit of AD pathogenesis, causes mTOR hyperactivity by

208 anscription elongation to mRNA transport, as culprit of aggressive human breast cancers.

209 inding effective inhibitors against HIV, the culprit of AIDS (acquired immunodeficiency syndrome).

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

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

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

217 Nicotine (Nic) is a likely culprit of pathobiological effects because it displaces

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 (AD) patients and is regarded by many as the culprit of the disorder.

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

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

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

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

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

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

227 cacy of nonculprit multivessel compared with culprit-only stenting in patients with multivessel disea

228 479 underwent multivessel and 761 underwent culprit-only stenting.

229 nce of the composite end point compared with culprit-only stenting.

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

231 was treated with an antibiotic to which the culprit pathogen was resistant in vitro.

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

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

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

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

236 Culprit plaques had a higher degree of contrast enhancem

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

238 OCT imaging was performed at culprit and non-culprit plaques in patients presenting with stable angin

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

240 The culprit plaques often demonstrate large plaque and necro

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

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

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

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

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

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

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

248 ions suggest that persisters may be the main culprit responsible for the recalcitrance of chronic inf

249 ulprit, the post PCI, and nonculprit values (culprit sIMR 26.68+/-2.06, nonculprit sIMR 18.37+/-1.89,

250 taneous intervention sIMR 18.5+/-1.94 versus culprit sIMR 26.68+/-2.06, P<0.0001).

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

252 Vessel healing at the culprit site in AMI patients treated with DES is substan

253 ach failed to detect increased signal at the culprit site in nearly half of AMI patients, highlightin

254 S is substantially delayed compared with the culprit site in patients receiving DES for stable angina

255 were significantly greater compared with the culprit site in stable patients (neointimal thickness: 0

256 We compared the response to stenting at the culprit site in these 2 groups and to nonculprit sites w

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

258 Although neointimal thickness in the AMI culprit site was significantly less (median, 0.04 mm; in

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

260 esses that determine recurrent events at non-culprit sites.

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

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

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

264 vated BNP levels are associated with tighter culprit stenosis, higher CTFC, and LAD involvement.

265 theses for elucidating the neurobiology of a culprit subcortical network.

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

267 cleus has been suggested to be the molecular culprit that confers cellular toxicity in the neurodegen

268 meability caused by alcohol ingestion as the culprit that leads to endotoxemia.

269 ed in the mast cell releasates as the likely culprits that digest these cytokines.

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

271 ificant difference in IMR values between the culprit, the post PCI, and nonculprit values (culprit sI

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

273 Although a culprit thrombotic lesion may be treated effectively by

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

275 ergence of autoreactivity is likely the main culprit underlying long-term islet graft failure, and ne

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

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

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

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

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

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

282 Patients with BNP >80 pg/ml had tighter culprit vessel stenosis on quantitative coronary angiogr

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

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

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

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

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

288 ot affect the entire supply territory of the culprit vessel.

289 nt (median CTFC 43 vs. 30, p = 0.018) in the culprit vessel.

290 Angiography was used to determine culprit vessel.

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

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

293 Performing culprit-vessel primary percutaneous coronary interventio

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

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

296 may bring about more accurate assignment to culprit vessels and thus improved guidance and monitorin

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.