ライフサイエンスコーパス: Clostridium

1 sed Bacteroidetes and Firmicutes but reduced Clostridium.

2 The enzyme, Clostridium acetobutylicum (CaADH), recently expressed b

3 ular complexes between CdSe nanocrystals and Clostridium acetobutylicum [FeFe] hydrogenase I (CaI) en

4 Clostridium acetobutylicum is a bacterial species that f

5 olyketides native to the anaerobic bacterium Clostridium acetobutylicum, an organism well-known for i

6 cetone-butanol-ethanol (ABE) fermentation by Clostridium acetobutylicum, during which cells convert c

7 ogenases, from Chlamydomonas reinhardtii and Clostridium acetobutylicum, react with O2 according to t

8 henotype compared to controls, a decrease in Clostridium and an increase in Enterobacter, Escherichia

9 Two fecal microbiota signatures (Clostridium and Klebsiella OTUs) and need for prolonged

10 Anaerobic bacteria, such as Clostridium and Salmonella, can selectively invade and c

11 y higher relative abundances of Veillonella, Clostridium, Bacteroides, Lactobacillus, Collinsella and

12 From 1976 to 2016, neurotoxigenic Clostridium baratii type F caused 18 (<0.5%) reported US

13 Degenerate Clostridium beijerinckii strain (DG-8052) can be partial

14 um cluster XIVa species Blautia producta and Clostridium bolteae restores colonization resistance aga

15 ial protein, transcription terminator Rho of Clostridium botulinum (Cb-Rho), could form a prion.

16 Laboratory testing was performed for Clostridium botulinum and botulinum neurotoxin.

17 Here the Clostridium botulinum C2 binding/translocation domain wa

18 The natural Clostridium botulinum C2 toxin was then delivered to hum

19 Clostridium botulinum produces botulinum neurotoxins (Bo

20 Only Clostridium botulinum strain IBCA10-7060 produces the re

21 Clostridium botulinum strain IBCA10-7060 was recently re

22 Rarely, Clostridium botulinum strains that produce two serotypes

23 ne of seven highly potent toxins produced by Clostridium botulinum which inhibit neurotransmission at

24 linum neurotoxins, produced by the bacterium Clostridium botulinum, act on their hosts by a high-affi

25 kholderia mallei, Burkholderia pseudomallei, Clostridium botulinum, Brucella melitensis, Brucella abo

26 hewanella oneidensis, Shewanella woodyi, and Clostridium botulinum, indicating that the binding site

27 ll-characterized butyrate-producing bacteria Clostridium butyricum CGMCC0313.1 (CB0313.1) on hypergly

28 e of botulism in the United States caused by Clostridium butyricum type E.

29 Clostridium butyricum was specifically associated with N

30 e polymerase chain reaction (qPCR) assay for Clostridium butyricum, and we tested stool samples from

31 ty to the GRE-type glycerol dehydratase from Clostridium butyricum, we demonstrate that the RiDD is i

32 bundant anaerobic solvent-producing bacteria Clostridium carboxidivorans is likely responsible for el

33 elineation and metabolite turnover rates) of Clostridium carboxidivorans P7, a model strain for indus

34 (C. thermocellum) as well as to non-cognate Clostridium cellulolyticum dockerin.

35 ay be conserved among other starch-degrading Clostridium cluster XIVa organisms in the human gut.

36 cterium species, Sutturella wadsworthia, and Clostridium cluster XIVa organisms, and at the same time

37 sortium of commensal bacteria containing the Clostridium cluster XIVa species Blautia producta and Cl

38 remission was associated with proportions of Clostridium clusters IV and XIVa.

39 reaction of fecal samples for Bacteroidetes, Clostridium clusters XIVa and IV, and C. difficile were

40 sis characterized by increased proportion of Clostridium coccoides (cluster XIVa), C coccoides-Eubact

41 Quality control ranges for Clostridium difficile (0.12 to 1 mug/ml) and Eggerthella

42 nfective aetiology (112/1207 (9.2%)) such as Clostridium difficile (97/1048 (9.3%) tested) or virolog

43 No effect was observed on incidence of Clostridium difficile (OR 1.02, 95% CI 0.34-3.01), and m

44 Clostridium difficile (Peptoclostridium difficile) is a

45 xin (CTB5) and a subfragment of toxin A from Clostridium difficile (TcdA-A2).

46 Clostridium difficile 027/NAP1/BI is the most common C.

47 mice datasets, investigating infection with Clostridium difficile and an immune-modulatory probiotic

48 TcdB) are produced by the bacterial pathogen Clostridium difficile and are responsible for the pathol

49 (endospores), such as those of the pathogens Clostridium difficile and Bacillus anthracis, are unique

50 outcomes of hospitalized patients tested for Clostridium difficile and determine the correlation betw

51 Herein, we establish Clostridium difficile and its enterotoxin A (TcdA) as Py

52 nzymatic activity of DisA-like proteins from Clostridium difficile and Methanocaldococcus jannaschii.

53 applies to the CD27L endolysin that targets Clostridium difficile and the CS74L endolysin that targe

54 ssociation of proton pump inhibitor use with Clostridium difficile and ventilator-associated pneumoni

55 a key prevention strategy for resistance and Clostridium difficile Antibiotic stewardship programs (A

56 In the Clostridium difficile cell wall protein family, we show

57 ctobacilli in the course of her treatment of Clostridium difficile colitis.

58 The diarrheal pathogen Clostridium difficile consists of at least six distinct

59 There is no stand-alone Clostridium difficile diagnostic that can sensitively an

60 an acquire multidrug-resistant organisms and Clostridium difficile from inadequately disinfected envi

61 eliable tools for the detection of toxigenic Clostridium difficile from unformed (liquid or soft) sto

62 In the past decade Clostridium difficile has become a bacterial pathogen of

63 Clostridium difficile has become one of the most common

64 Unlike in B. subtilis, SpoIIQ of Clostridium difficile has intact LytM zinc-binding motif

65 and metagenomic shotgun sequencing (MSS) for Clostridium difficile identification in diarrhea stool s

66 , drug-product-related impurities of an anti-Clostridium difficile IgG1 mAb drug substance were profi

67 The role of Clostridium difficile in causing disease in infants is u

68 The horizontal transmission of Clostridium difficile in the hospital environment is dif

69 Drivers of differences in Clostridium difficile incidence across acute and long-te

70 were rated >6 in all criteria: 2 measures of Clostridium difficile incidence, incidence of drug-resis

71 h daptomycin (MIC90 0.5 vs 2 mug/mL) against Clostridium difficile including NAP1 epidemic strains.

72 zole: 2), and one patient was diagnosed with Clostridium difficile infection (0 vs 1).

73 ently encountered infectious etiologies were Clostridium difficile infection (13.3% and 11.8%, respec

74 plification tests (NAATs) do not distinguish Clostridium difficile infection (CDI) and asymptomatic C

75 e advances in the diagnosis and treatment of Clostridium difficile infection (CDI) and prevention eff

76 es suggest that most cases of hospital-onset Clostridium difficile infection (CDI) are unrelated to o

77 methods may underestimate the true burden of Clostridium difficile infection (CDI) because they fail

78 Clostridium difficile infection (CDI) can cause severe d

79 Little is known about pediatric Clostridium difficile infection (CDI) epidemiology.

80 Clostridium difficile infection (CDI) following antibiot

81 Recurrent or refractory Clostridium difficile infection (CDI) has become an incr

82 icrobiota transplantation (FMT) in recurrent Clostridium difficile infection (CDI) has been limited t

83 Patients with recurrent Clostridium difficile infection (CDI) have a >/=60% risk

84 Since 2000, the incidence and severity of Clostridium difficile infection (CDI) have increased.

85 The currently available diagnostics for Clostridium difficile infection (CDI) have major limitat

86 id suppression medication is associated with Clostridium difficile infection (CDI) in adults and is i

87 dies on risk factors for and transmission of Clostridium difficile infection (CDI) in China have been

88 Clostridium difficile infection (CDI) is a frequent comp

89 Clostridium difficile infection (CDI) is a major burden

90 Clostridium difficile infection (CDI) is a major cause o

91 Clostridium difficile infection (CDI) is an important ho

92 Clostridium difficile infection (CDI) is associated with

93 Clostridium difficile infection (CDI) is common after li

94 Clostridium difficile infection (CDI) is facilitated by

95 mal therapy for critically ill patients with Clostridium difficile infection (CDI) is not known.

96 f fecal microbiota transplantation (FMT) for Clostridium difficile infection (CDI) is not well-known.

97 Managing recurrent Clostridium difficile infection (CDI) presents a signifi

98 Variation in Clostridium difficile infection (CDI) rates between heal

99 This study analyzes and reports Clostridium difficile infection (CDI) rates, risk factor

100 innate immune response to the resolution of Clostridium difficile infection (CDI) remains incomplete

101 Clostridium difficile infection (CDI) represents an impo

102 for the efficacy of probiotics in preventing Clostridium difficile infection (CDI), but guidelines do

103 (FT) is a promising treatment for recurrent Clostridium difficile infection (CDI), but its true effe

104 Unfortunately, the rise of Clostridium difficile infection (CDI), particularly in e

105 Clostridium difficile infection (CDI), the most common h

106 es have evaluated risk factors for recurrent Clostridium difficile infection (CDI), the vast majority

107 ens, including acute kidney injury (AKI) and Clostridium difficile infection (CDI), were also conside

108 rope and the United States for patients with Clostridium difficile infection (CDI).

109 considered important for protection against Clostridium difficile infection (CDI).

110 e to severe disease and treatment failure in Clostridium difficile infection (CDI).

111 is a highly effective therapy for recurrent Clostridium difficile infection (CDI).

112 ease states, and the prototypical example is Clostridium difficile infection (CDI).

113 is a highly effective therapy for recurrent Clostridium difficile infection (CDI).

114 peutic effects of dietary supplementation on Clostridium difficile infection (CDI).

115 -Counterpoint on the laboratory diagnosis of Clostridium difficile infection (CDI).

116 h care-onset health care facility-associated Clostridium difficile infection (HO-CDI) is overdiagnose

117 actam (PIP/TAZO) shortage and hospital-onset Clostridium difficile infection (HO-CDI) risk in 88 US m

118 Recurrent Clostridium difficile infection (RCDI) is associated wit

119 ed hospitalization, and hospitalization with Clostridium difficile infection [CDI]) were associated w

120 Clostridium difficile infection after LT was associated

121 ts it has been successfully used in cases of Clostridium difficile infection and IBD, although contro

122 We also assessed rates of Clostridium difficile infection and potential allergic r

123 ctors affecting a person's susceptibility to Clostridium difficile infection are well-understood, lit

124 s is not observed in subjects with recurrent Clostridium difficile infection but is observed in the s

125 Clostridium difficile infection causes severe complicati

126 The incidence of Clostridium difficile infection has increased among chil

127 Clostridium difficile infection in LT recipients was ass

128 We compared rates of recurrent Clostridium difficile infection in patients receiving or

129 The detection and diagnosis of Clostridium difficile infection in pediatric populations

130 The magnitude and scope of Clostridium difficile infection in the United States con

131 Clostridium difficile infection is a growing problem in

132 Their use as probiotics for prevention of Clostridium difficile infection is prevalent among consu

133 Clostridium difficile infection is the leading cause of

134 Clostridium difficile infection is the leading cause of

135 Clostridium difficile infection is the most common healt

136 Clostridium difficile infection occurred in 27 (14%) of

137 Clostridium difficile infection often occurred soon afte

138 reports found addressed the use of FMTs for Clostridium difficile infection or inflammatory bowel di

139 Whereas many antibiotics increase risk of Clostridium difficile infection through dysbiosis, epide

140 cohort of 109 subjects treated for recurrent Clostridium difficile infection with fecal microbiota tr

141 t serious cephalosporin-associated ADRs were Clostridium difficile infection within 90 days (0.91%),

142 with outcomes (antibiotic-days, incidence of Clostridium difficile infection, and in-hospital mortali

143 viously used to cure patients with recurrent Clostridium difficile infection, could also protect agai

144 for the same infection, acute kidney injury, Clostridium difficile infection, or drug-related adverse

145 py, and frequency of complications including Clostridium difficile infection, readmission, and all-ca

146 acious and inexpensive therapy for recurrent Clostridium difficile infection, yet its safety is thoug

147 ns about promoting antibiotic resistance and Clostridium difficile infection.

148 mycin antibiotic treatment and opportunistic Clostridium difficile infection.

149 contributes to the pathology observed during Clostridium difficile infection.

150 nsecutive, evaluable patients with recurrent Clostridium difficile infection.

151 and fidaxomicin are therapies of choice for Clostridium difficile infection.

152 or-associated complication or pneumonia, and Clostridium difficile infection; minor outcomes included

153 BACKGROUND & AIMS: Studies of Clostridium difficile infections (CDIs) among individual

154 al microbiota transplantation to face severe Clostridium difficile infections and to perform decoloni

155 biotic-based strategies for the treatment of Clostridium difficile infections disrupt indigenous micr

156 The prevalence of Clostridium difficile infections has increased due to th

157 The control of Clostridium difficile infections is an international cli

158 han 9000 nosocomial infections, 1000 to 5000 Clostridium difficile infections, and 2 to 6 cases of an

159 den of antimicrobial-resistant organisms and Clostridium difficile infections, halting unnecessary an

160 Clostridium difficile is a clinically significant pathog

161 Clostridium difficile is a gastrointestinal pathogen but

162 Clostridium difficile is a major nosocomial pathogen tha

163 Clostridium difficile is a major, life-threatening hospi

164 jor cause of antibiotic-associated diarrhea, Clostridium difficile is a serious problem in health car

165 Clostridium difficile is a significant concern as a noso

166 Clostridium difficile is an anaerobic pathogen that form

167 Clostridium difficile is currently the leading cause of

168 ecal toxin negative (FT-) in transmission of Clostridium difficile is currently unknown.

169 The pathogenicity of Clostridium difficile is linked to its ability to produc

170 Clostridium difficile is the cause of antibiotics-associ

171 Clostridium difficile is the most common cause of health

172 Clostridium difficile is the most common hospital acquir

173 Clostridium difficile is the most commonly reported noso

174 Clostridium difficile is the most frequently identified

175 Clostridium difficile is the most important enteropathog

176 Clostridium difficile is the principal cause of nosocomi

177 rienced a major outbreak associated with the Clostridium difficile NAP1/027/BI strain.

178 Diarrhoea positive for Clostridium difficile occurred in two patients (<1%) in

179 ed in colonic neurons of human patients with Clostridium difficile or ulcerative colitis.

180 on of spores is critical for the survival of Clostridium difficile outside the host gastrointestinal

181 Clostridium difficile PCR ribotype 265 (toxin A negative

182 orders for ovum and parasite (O&P) exams and Clostridium difficile PCR.

183 ACKGROUND & AIMS: Nosocomial infections with Clostridium difficile present a considerable problem des

184 w that toxins A or B of the enteric pathogen Clostridium difficile recapitulate the salient features

185 Clostridium difficile remains the leading cause of nosoc

186 obiota, which consequently enables toxigenic Clostridium difficile species to proliferate and cause i

187 hotspots associated with mobile elements in Clostridium difficile ST6 and a previously undescribed 3

188 Clostridium difficile strain BI/NAP1/027 is associated w

189 Clostridium difficile strains within the hypervirulent c

190 Hypervirulent Clostridium difficile strains, which are associated with

191 Clostridium difficile TcdB (2366 amino acid residues) is

192 TcdB is one of the key virulence factors of Clostridium difficile that is responsible for causing se

193 n that we identified from the human pathogen Clostridium difficile The crystal structure shows that t

194 Clostridium difficile toxin B (TcdB) is a critical virul

195 or Pyrin inflammasomes by nigericin (NG) or Clostridium difficile toxin B (TcdB), respectively.

196 Clostridium difficile toxin was subsequently detected in

197 ve and quantitative methods for detection of Clostridium difficile toxins provide new tools for diagn

198 ty, produce the actin-ADP ribosylating toxin Clostridium difficile transferase (CDT).

199 y additionally produce the binary CDT toxin (Clostridium difficile transferase) that ADP-ribosylates

200 Accurate tracking of Clostridium difficile transmission within healthcare set

201 for treatment of recurrent infections (i.e., Clostridium difficile) in the human gut and as a general

202 inococcus obeum, Salmonella typhimurium, and Clostridium difficile) to quantify, expand, and characte

203 g activity in vivo against Shiga, botulinum, Clostridium difficile, anthrax, and ricin toxins.

204 In the intestinal pathogen Clostridium difficile, c-di-GMP inhibits flagellar motil

205 Many factors may cause diarrhoea, including Clostridium difficile, drugs (e.g. laxatives, antibiotic

206 s that are not reported at this institution (Clostridium difficile, enteroaggregative Escherichia col

207 ntamination, colonization, or infection with Clostridium difficile, methicillin-resistant Staphylococ

208 ts to the health service and predisposing to Clostridium difficile, methicillin-resistant Staphylococ

209 pansion of several potential pathogens (e.g. Clostridium difficile, Salmonella, and Escherichia coli)

210 ansplantation led to resolution of recurrent Clostridium difficile, significantly decreased recurrent

211 infections (HAIs), including those caused by Clostridium difficile, Staphylococcus aureus, Pseudomona

212 his setting, such as Cryptosporidiumspp. and Clostridium difficile, were detected with the GPP.

213 d mortality rates associated with nosocomial Clostridium difficile-associated diarrhea (CDAD), a seri

214 r expressing the HIV-1-derived Gag Ag or the Clostridium difficile-derived toxin B resulted in signif

215 fluence susceptibility to pathogens, such as Clostridium difficile.

216 re-forming pathogens, Bacillus anthracis and Clostridium difficile.

217 a, Eggerthella, and the potential pathobiont Clostridium difficile.

218 ation among LFAs for influenza, malaria, and Clostridium difficile.

219 and TcdB are the major virulence factors of Clostridium difficile.

220 nzyme, SrtB, is conserved between strains of Clostridium difficile.

221 of TcdB varies between different strains of Clostridium difficile.

222 tion resistance against pathogens, including Clostridium difficile.

223 In mattress dust, the genera Clostridium, Facklamia, an unclassified genus within the

224 Bacteria of the genera Bacillus and Clostridium form highly resistant spores, which in the c

225 Chath_Est1 from the anaerobic risk 1 strain Clostridium hathewayi DSM-13479 was found to hydrolyze P

226 tective effects of F. prausnitzii A2-165 and Clostridium hathewayi, a low secretor of IL-10, on the T

227 -weaned rats to harbor significantly lowered Clostridium histolyticum bacterial groups but exhibit ma

228 collagenase H (ColH) from the human pathogen Clostridium histolyticum.

229 both the Bacteroides-Prevotella spp. and the Clostridium-histolyticum groups, and increased the short

230 microbial culture techniques, we discovered Clostridium immunis, a previously unknown bacterial spec

231 hol or carboxylate, with a strain related to Clostridium kluyveri dominating the enrichments.

232 as the metabolism of the anaerobic bacterium Clostridium kluyveri, which I took on in 1965 in Karl De

233 accompanied with the decreased abundance of Clostridium, Lactobacillus, Desulfovibrio, and Methyloba

234 Clostridium ljungdahlii derives energy by lithotrophic a

235 As a proof-of-concept, Clostridium ljungdahlii was engineered to produce aceton

236 , Dorea (log2 fold change -1.65, P=.02), and Clostridium (log2 fold change -1.47, P=.002) were underr

237 nd 78 controls showed an association between Clostridium neonatale and Staphylococcus aureus with NEC

238 CBS-PPases of Desulfitobacterium hafniense, Clostridium novyi, and Clostridium perfringens and incre

239 coccus faecalis, Lactobacillus crispatus and Clostridium orbiscindens) promote resistance to lung inf

240 A specific human-associated gut microbe, Clostridium orbiscindens, produced DAT and rescued antib

241 PH-driven assay and while characterizing the Clostridium pasteurianum (Cp) [FeFe] hydrogenase, CpI, w

242 6S and C60S variants of the thioredoxin-like Clostridium pasteurianum [Fe2S2] ferredoxin (CpFd) provi

243 From a library of 10 080 randomly mutated Clostridium pasteurianum [FeFe] hydrogenases, we found a

244 from Chlamydomonas reinhardtii and CpI from Clostridium pasteurianum, are very similar, despite larg

245 itrogenases (Azotobacter vinelandii, Av, and Clostridium pasteurianum, Cp) at pHs between 4.5 and 8.

246 An [FeFe]-hydrogenase from Clostridium pasteurianum, CpI, is a model system for bio

247 ter," and CpI from the fermentative anaerobe Clostridium pasteurianum, which contains four low-potent

248 The presence and abundance of Clostridium perfringens (8.4%) and Bacteroides dorei (0.

249 cross-react with a homologous sequence of a Clostridium perfringens adenosine triphosphate-binding c

250 obacterium hafniense, Clostridium novyi, and Clostridium perfringens and increase their activity up t

251 Clostridium perfringens can produce up to three differen

252 P = .1 and P = .01 for consecutive samples); Clostridium perfringens continued to be more prevalent i

253 A noncytotoxic C-terminal fragment of Clostridium perfringens enterotoxin (cCPE) is a natural

254 Clostridium perfringens enterotoxin (CPE) causes food po

255 A published complex of Clostridium perfringens GH125 enzyme with a nonhydrolyza

256 acillus anthracis, Campylobacter jejuni, and Clostridium perfringens IMPDHs.

257 Necrotic enteritis (NE) caused by Clostridium perfringens is one of the most detrimental i

258 ysis, we were able to identify inhibitors of Clostridium perfringens neuraminidase present in a root

259 Many Clostridium perfringens strains produce NanI as their ma

260 2-aminobenzoic acid using neuraminidase from Clostridium perfringens that cleaves sialic acid monomer

261 peL is a recently identified LCT produced by Clostridium perfringens that has received relatively lim

262 Culture confirmed the presence of Clostridium perfringens type A.

263 Clostridium perfringens type D strains cause enterotoxem

264 ia (FIBs; Escherichia coli, enterococci, and Clostridium perfringens) exhibited biphasic decay patter

265 C. difficile was codetected with Clostridium perfringens, norovirus, sapovirus, parechovi

266 ort how the plant fermenting, soil bacterium Clostridium phytofermentans enhances growth on cellulose

267 ell walls by the cellulolytic soil bacterium Clostridium phytofermentans produces toxic aldehyde inte

268 s in transcription start site (TSS) usage by Clostridium phytofermentans, a model bacterium for ferme

269 Using these platforms, we determine that Clostridium scindens, a bile acid 7alpha-dehydroxylating

270 d a temporal succession from highly abundant Clostridium sensu stricto to Psychrosinus.

271 In ileal samples, the genus Clostridium sensu stricto was dramatically reduced in th

272 st of MGS enriched in the H7N9 patients were Clostridium sp. 7 2 43FAA and Enterococcus faecium.

273 e present in other pathogenic and industrial Clostridium species and may represent a key regulatory p

274 he intestinal tract by Citrobacter freundii, Clostridium species, Enterobacter cloacae, Enterococcus

275 ng a remarkable predominance of Serratia and Clostridium species, which switched from asymptomatic gu

276 n in other spore forming bacteria, including Clostridium species.

277 characterize a pathway from the gut symbiont Clostridium sporogenes that generates aromatic amino aci

278 fficile and the CS74L endolysin that targets Clostridium sporogenes.

279 in multiple pathogenic Bacteroides spp. and Clostridium spp.

280 ties converged, and consistent enrichment of Clostridium spp. was observed, independent of the suppli

281 ent) of Escherichia coli, Bacillus spp., and Clostridium spp. were greater >/=2.5-fold in volunteers

282 Clostridium spp., Bacteroides uniformis, Christensenella

283 n the human body are the obligate anaerobes, Clostridium spp., in the internal postmortem microbial c

284 sing enzymes cellodextrin phosphorylase from Clostridium stercorarium or Clostridium thermocellum as

285 e picture of how the active site of LAM from Clostridium subterminale SB4 "tames" the 5'-dAdo* radica

286 wo invasive species, Ruminococcus gnavus and Clostridium symbiosum, to the microbiota from undernouri

287 ntable disease caused by a toxin produced by Clostridium tetani-a Gram-positive bacillus found in hig

288 osphorylase from Clostridium stercorarium or Clostridium thermocellum as catalyst.

289 he sactionine bond-forming enzyme CteB, from Clostridium thermocellum ATCC 27405, with both SAM and a

290 Clostridium thermocellum can ferment cellulosic biomass

291 the contribution of distinct residues at the Clostridium thermocellum cohesin-dockerin interface to b

292 Clostridium thermocellum could potentially be used as a

293 t under native conditions wild-type Doc from Clostridium thermocellum exocellulase Cel48S populates b

294 we present crystal structures of PCAT1 from Clostridium thermocellum in two different conformations.

295 s in BiFae1B with the feruloyl esterase from Clostridium thermocellum suggest that both domains lack

296 ons to derive the genomic TU organization of Clostridium thermocellum using a machine-learning approa

297 hieved by the method on Escherichia coli and Clostridium thermocellum, substantial work is needed to

298 recombinant bacterial minicellulosomes from Clostridium thermocellum, we demonstrate the ability to

299 f the activated endolysin CTP1L that targets Clostridium tyrobutyricum, consisting of a complex betwe

300 , including Anaeroplasma, Campylobacter, and Clostridium, were correlated with apparent CF digestibil