ライフサイエンスコーパス: dextrose

1 mmol/L sodium and 20 mmol/L potassium in 5% dextrose).

2 pon restoration of ATP levels by addition of dextrose.

3 dration is often treated more slowly with 5% dextrose.

4 days' postfeeding with ethanol, but not with dextrose.

5 ) achieved by intra-arterial infusion of 50% dextrose.

6 d in groups fed unsaturated fatty acids with dextrose.

7 iets containing either ethanol or isocaloric dextrose.

8 hat were pair-fed with isocaloric amounts of dextrose.

9 d to 90% hepatectomy (Hpx) and given 5% oral dextrose.

10 that ethanol was isocalorically replaced by dextrose.

11 RNA targets in the fermentable carbon source dextrose.

12 lt, d-(+)-galactose, sorbitol, glycerol, and dextrose.

13 rbonate-buffered solutions that contained 4% dextrose.

14 red in Adsol or EAS 25 (mmol/L: adenine 2/2, dextrose 122/110, mannitol 42/55, glycerol 0/150, NaCl 1

15 g(-1) x min(-1)) and left intrarenal [6,6-2H]dextrose (14 micromol x kg(-1) x min(-1)) to achieve and

16 in cells treated with high concentrations of dextrose, 2) statin treatment of endothelial cells norma

17 in dextrose 5% in water, n = 84) or placebo (dextrose 5% in water only, n = 83) every 6 hours for 96

18 travenous infusion of vitamin C (50 mg/kg in dextrose 5% in water, n = 84) or placebo (dextrose 5% in

19 om-limited treadmill exercise testing during dextrose 5% infusion and after double-blind intravenous

20 eceive NAC 21 g (~300 mg/kg) for 20 hours or dextrose 5%.

21 ours of hyperglycemia (300 mg/dL) created by dextrose (50%) intra-arterial infusion, and with coadmin

22 In plasma prepared with acid citrate dextrose a binding pattern identical to that of serum wa

23 d samples collected in EDTA and acid-citrate-dextrose (ACD) were compared by cytomegalovirus (CMV) pp

24 IV-1-infected patients in EDTA, acid citrate dextrose (ACD), and heparin tubes, aliquoted, and stored

25 etected in EDTA-, heparin-, and acid citrate dextrose (ACD)-anticoagulated plasma samples were compar

26 in(-1)) with a variable infusion of [6-(2)H2]dextrose adjusted to maintain plasma glucose at either a

27 atio, 2.2; 95% CI, 1.9-2.7; p < 0.0001), and dextrose (adjusted odds ratio, 2.8; 95% CI, 2.3-3.4).

28 Hyperglycemia was induced by intraperitoneal dextrose administration prior to ischemia.

29 The only predictor of hyperglycemia was a dextrose administration rate >4 mg/kg/min.

30 PN regimens should not exceed a dextrose administration rate of 4 mg/kg/min to avoid hyp

31 h culture grown at 30 degrees C on Sabouraud dextrose agar (Emmons modification) by following the rec

32 occus neoformans using 2% dextrose Sabouraud dextrose agar (SabDex) with fluconazole was compared to

33 ain heart infusion agar (BHI), and Sabouraud dextrose agar (SDA) and into a BACTEC 13A bottle.

34 38 isolates grown on prepoured BBL Sabouraud dextrose agar (SDA) and prepoured Remel SDA.

35 Paired Sabouraud dextrose agar (SDA) plates were always positive for fung

36 specimens were streaked onto CAC, Sabouraud dextrose agar (SDA), inhibitory mold agar (IMA), and Myc

37 ia, inhibitory mold agar (IMA) and Sabouraud dextrose agar (SDA), were compared with respect to recov

38 (USP<71>, BacT/Alert, Bactec, and Sabouraud dextrose agar [SDA] culture), three different bottle med

39 lysis, yeasts were inoculated onto Sabouraud dextrose agar and incubated at 28 degrees C for 24 h.

40 ast isolates were subcultured onto Sabouraud dextrose agar and were incubated at 28 degrees C for 24

41 d on double-pour agar plates by using potato dextrose agar in both.

42 Each scraping was inoculated onto Sabouraud Dextrose Agar in C-shaped streaks and incubated at 25 de

43 the same isolate of yeast grown on Sabouraud dextrose agar simultaneously.

44 posing 90 mm settle plates containing potato dextrose agar to the air for 10 min.

45 Germinated fungal spores on potato dextrose agar were also reduced after plasma treatment.

46 ve fungal culture media, including Sabouraud dextrose agar with gentamicin (SDA), inhibitory mold aga

47 agar, sheep blood chocolate agar, Sabouraud dextrose agar, brain heart infusion, thioglycolate broth

48 on a variety of substrates including potato dextrose agar, olive oil, glyceride trioleate, oleic aci

49 ains were grown at 37 degrees C on Sabouraud dextrose agar, only C. dubliniensis strains coaggregated

50 ly, at 37 degrees C on yeast extract-peptone-dextrose agar, suggesting that T6P accumulation in R265t

51 Isolates were grown on Sabouraud-Dextrose agar, swabbed, and prepared in suspension, and

52 sing three different cereal agars and potato dextrose agar.

53 fied equally as well as those from Sabouraud dextrose agar.

54 strains passaged on CHROMagar and on potato dextrose agar.

55 tration of perfluorocarbon-exposed sonicated dextrose albumin (PESDA) and transcutaneous delivery of

56 ously that perfluorocarbon-exposed sonicated dextrose albumin (PESDA) microbubbles bind to injured va

57 trast agent perflurocarbon exposed sonicated dextrose albumin (PESDA) to increase uptake of VEGF in t

58 ntravenous perfluorocarbon-exposed sonicated dextrose albumin contrast injection.

59 ections of perfluorocarbon-exposed sonicated dextrose albumin microbubble contrast medium in humans.

60 ntravenous perfluorocarbon-exposed sonicated dextrose albumin, and ultrasound can be significantly im

61 andard PN containing conventional amounts of dextrose, amino acids, micronutrients, and lipid (120 kJ

62 DTIC 220 mg/m(2) IV for 1 hour in 500 mL of dextrose and (1/2) NaCl on days 1 to 3 of a 3-week cycle

63 ously (IV) for 30 to 45 minutes in 500 mL of dextrose and (1/2) normal saline (NS) on days 1 to 3 of

64 rs (Mueller-Hinton agar supplemented with 2% dextrose and 0.5 microg/ml methylene blue [MGM], Shadomy

65 media (supplemented Mueller-Hinton agar [2% dextrose and 0.5 microg/ml methylene blue] and plain Mue

66 2) IV for 2 to 3 hours in 750 to 1,000 mL of dextrose and 5% water on day 1 of every odd 3-week cycle

67 ired blood samples collected in acid-citrate-dextrose and EDTA were compared for human immunodeficien

68 Rats were fed intragastrically ethanol or dextrose and either medium-chain triglycerides, corn oil

69 own on a mixed carbon source containing both dextrose and methanol, ubiquitin is found in small stora

70 was not significantly different between the dextrose and placebo gel groups (20.8% vs 18.7%; unadjus

71 was not significantly different between the dextrose and placebo groups (cognitive: 7.6% vs 5.3%; RD

72 Ume6p acetylation occurs in medium lacking dextrose and results in a partial destruction of the rep

73 ith fasting insulin (57 pmol/L), achieved by dextrose and somatostatin (octreotide) infusion (150 mg/

74 after which the stomach was loaded with acid dextrose and the recording continued for 2 hours with in

75 pid, 170 micromol h(-1), chylous lymph) or a dextrose and/or electrolyte solution (control lymph).

76 iet contained 30% of calories as ethanol (or dextrose) and 25% of calories as corn oil.

77 blood (anticoagulated with citrate-phosphate-dextrose) and crystalloid and observed for the next 6 or

78 ined on solidified (1.5% agar) RPMI 1640 (2% dextrose), and zone diameters were obtained on supplemen

79 18-, and 3-fold in deletion strains grown on dextrose, and 2-, 7-, and 5-fold in deletion strains gro

80 pH 4.5 to 8.0, low O2 tension, 0.1 to 0.3 M dextrose, and absence of iron for 2 h.

81 ne HDP-cCDV was synthesized, suspended in 5% dextrose, and injected into the rabbit's vitreous at 10,

82 gned infusions of either insulin at 2.5 U/h, dextrose, and potassium (GIK) or normal saline and potas

83 tion difficulty (epinephrine, midazolam, 10% dextrose, and sodium bicarbonate).

84 nhibitory mold, cornmeal, Czapek-Dox, potato dextrose, and V8 juice agars; all isolates were sequence

85 dia, standard RPMI 1640 (RPMI), RPMI with 2% dextrose, antibiotic medium 3 (M3), and M3 with 2% dextr

86 d by a variety of sugars, including sucrose, dextrose, arabinose, fructose, and maltose.

87 d, regardless of use of EDTA or acid citrate dextrose as anticoagulant, and despite the presence of t

88 on of deuterated glucose and infusion of 20% dextrose as required to maintain euglycemia.

89 und, and the fellow eye was injected with 5% dextrose as the control.

90 CR, and 3) HS + CR + PR with a hyperosmolar dextrose-based solution (Delflex 2.5%).

91 rin and amino acids; EDEN trial: a different dextrose-based solution, icodextrin and amino acids) and

92 ention group (IMPENDIA trial: combination of dextrose-based solution, icodextrin and amino acids; EDE

93 ution or standard PD solution (Dianeal 4.25% dextrose, Baxter).

94 ms were grown in two different media: potato dextrose broth (PDB) and waste brewery yeast, either alo

95 ch competitor were inoculated into Sabouraud dextrose broth and incubated at 37 degrees C with vigoro

96 ntrolled by a GAL1 promoter grew normally on dextrose but not on galactose medium.

97 ated to receive either 546C88 or placebo (5% dextrose) by intravenous infusion for up to 72 hrs.

98 H rather than acidifying it, as occurs after dextrose catabolism.

99 iluted drugs in 7H9 broth-oleic acid albumin dextrose catalase.

100 ller-Hinton broth with 5% oleic acid-albumin-dextrose-catalase and 7H9 broth with casein) and by macr

101 serum) is used instead of oleic acid-albumin-dextrose-catalase to support good growth of M. tuberculo

102 s, the sensor has been characterized for the dextrose concentration range of 0 mM-10mM including the

103 trition, parenteral nutrition, propofol, and dextrose containing fluids were collected for 7 days fol

104 oglycemia that was managed with concentrated dextrose containing fluids.

105 If alcoholic ketoacidosis is suspected, dextrose-containing fluids are recommended over normal s

106 t the 3' end of the GAL10 coding sequence in dextrose-containing growth medium that induces antisense

107 ubsequently, yeast cells were transferred to dextrose-containing growth medium to stop HO expression,

108 itrate-dextrose regional anticoagulation and dextrose-containing replacement fluids in the CVVH circu

109 (BCDTP) (collected in EDTA- or acid citrate dextrose-containing tubes in 1996 and 1997, had a 2-h ma

110 atin (sufficient to induce neurotoxicity) or dextrose control injections.

111 n the presence of ethanol (ethanol group) or dextrose (control group).

112 withdrawal, were refed ethanol or isocaloric dextrose (control) diets intragastrically for 7 days.

113 volume bolus and intravenous infusions of 5% dextrose (control, n = 8).

114 atectomy model in mice given standard or 10% dextrose (D10)-supplemented drinking water.

115 .p.) 60 min after DZ deposits, but not after dextrose deposits, further reduced the MRF-evoked EMG re

116 After 5 d of drinking 5% dextrose, desmopressin does not increase the osmolality

117 Main-trial test meals were dextrose, dextrose plus 10 g lactulose, plain hot rice,

118 s; both Sod1(+/+) and Sod1(-/-) mice fed the dextrose diet had normal histology.

119 For comparing icodextrin and 4.25% dextrose during the long dwell of automated peritoneal d

120 Masking was achieved by infusion of 5% dextrose (during acetylcysteine delivery) or saline (for

121 ropine, bicarbonate, calcium, magnesium, and dextrose each year were calculated in patients with shoc

122 Flooding the field with non-ionic dextrose eliminates alternative current paths.

123 polymerization (DP; liquid chromatography), dextrose equivalency (reducing sugar assays), and preval

124 corn syrup solids glucose polymers used had dextrose equivalent (DE) values of 17 or 38, respectivel

125 synthesized by coupling maltodextrin with a dextrose equivalent of 19 to vitamin E succinate.

126 The Dextrose Equivalent value, which is a measure of starch

127 n previously optimized for concentration and dextrose equivalents (n = 57), and to mask texture cues

128 ferences between the quantities of calories, dextrose, fat, and protein provided to the two groups.

129 were not significantly different between the dextrose-fed controls and saturated fat/ethanol-fed rats

130 omparison of symptoms during the lactose and dextrose feeding periods showed no significant differenc

131 er 15 mins and then 50 mg/kg in 250 mL of 5% dextrose for 45 mins at an infusion rate of 62.5 mL/hr.

132 LCTs alone or 100% of nonprotein energy from dextrose for 6 or 12 d.

133 sponse was assessed by the administration of dextrose for 80 min following a 4-h clamp with either sa

134 ransporters, icodextrin is superior to 4.25% dextrose for long-dwell fluid and solute removal.

135 arable at baseline (all patients using 4.25% dextrose for the long dwell) with regard to mean (+/-SEM

136 or anticoagulants (EDTA versus acid citrate dextrose) for either test.

137 medium (up to 23% of the cell dry weight in dextrose-free tryptic soy broth [TSB]).

138 Pilot-trial test meals were dextrose, freshly cooked polished rice, cooked rice cool

139 ) and the placebo group (n = 45) received 5% dextrose, from a minimum of 3 days up to a maximum of 5

140 neonatal hypoglycemia, prophylactic oral 40% dextrose gel at 1 hour of age, compared with placebo, re

141 However, the dextrose gel group had a significantly higher risk of mo

142 Prophylactic oral dextrose gel reduces neonatal hypoglycemia, but later be

143 on <22 mg/dL or <36 mg/dL despite 2 doses of dextrose gel) or recurrent hypoglycemia (>=3 episodes of

144 Control deposits of dextrose had no significant effect.

145 is of the Hypoglycaemia Prevention With Oral Dextrose (hPOD) randomized clinical trial was conducted.

146 yperglycemia was achieved by infusion of 50% dextrose (i.v.) prior to KCl-induced cardiac arrest glob

147 A solution of 5% dextrose in 0.9 % saline was continuously infused via fe

148 's solution (n = 6), 0.9% saline (n = 6), 5% dextrose in lactated Ringer's solution (D5RL) (n = 6), o

149 uperiority of icodextrin compared with 4.25% dextrose in optimizing peritoneal ultrafiltration (UF),

150 marate, separated by a 10-min infusion of 5% dextrose in sterile water, or three successive 10-min IV

151 unted, acute insulin response to intravenous dextrose in the patients with diffuse hyperinsulinism.

152 ated Ringer's solution (D5RL) (n = 6), or 5% dextrose in water (D5W) (n = 6).

153 avenous infusion of NAC (150 mg/kg/day in 5% dextrose in water [D5W]) or placebo (D5W) for up to 7 da

154 e (0.8 mg/kg ip) and were either starved (5% dextrose in water ad libitum) or fed (water and rat chow

155 ardial tamponade was induced by injecting 5% dextrose in water into the pericardial space until blood

156 a necessary mechanism for USV production, 5% dextrose in water or blood was infused intravenously int

157 -acetylcysteine at 150 mg/kg in 250 mL of 5% dextrose in water over 15 mins and then 50 mg/kg in 250

158 d divided into 3 groups: group I received 5% dextrose in water throughout the study period; group II

159 usion of normal saline (control; n=9) or 70% dextrose in water to increase blood glucose to 350 to 40

160 G-CSF or 5% dextrose in water was administered subcutaneously to cir

161 without a 2-microg/kg bolus) or placebo (5% dextrose in water) for 48 h in addition to their usual c

162 gnesium sulfate (2 g, 8 mmol) or placebo (5% dextrose in water) infused over 30 mins every 6 hrs for

163 Under control conditions (intracoronary 5% dextrose in water), atrial-pacing tachycardia decreased

164 renal interstitial infusions of vehicle (5% dextrose in water), cGMP (18, 36, and 72 mug/kg per minu

165 dy wt) and one after placebo administration (dextrose) in a double-blind randomized design.

166 s may be attributed to the inhibition of the dextrose-induced increase in superoxide anions, whereas

167 astatin (10 nmol/l) normalized the 500 mg/dl dextrose-induced permeability changes.

168 ative recovery of the liver was postponed in dextrose-infused mice (versus vehicle control) by an int

169 opolysaccharide (1 mg/kg) in the presence of dextrose infusion (100 microL/hr).

170 in levels increased significantly during the dextrose infusion (P<.001).

171 A regimen of parenteral dextrose infusion that delays PH-induced hypoglycemia fo

172 onset of hyperglycemia (10 mmol/l; variable dextrose infusion) under fixed hormonal conditions (soma

173 ma and p27 expression, was also disrupted by dextrose infusion.

174 00 mg/dL]), achieved by insulin and variable dextrose infusion; (2) hyperglycemia (12.5 mmol/L [225 m

175 ated by severe hypoglycemia and the need for dextrose infusion; C-peptide levels were initially low a

176 d to receive either midazolam or vehicle (5% dextrose) infusion for 6 hrs.

177 ly to groups that were given NAC or placebo (dextrose) infusion for 72 hours.

178 Acute hyperglycemia induced by dextrose ingestion does not restore their retinal functi

179 ination of media, which included Sabouraud's dextrose, inhibitory mold, cornmeal, Czapek-Dox, potato

180 f blood glucose less than 70 mg/dL where 50% dextrose injection was administered within 1 hour.

181 Hypertonic dextrose injections (prolotherapy) is an emerging treatm

182 ntrol animals were fed isocaloric amounts of dextrose instead of ethanol with the same diets.

183 Control rats received isocaloric amounts of dextrose instead of ethanol.

184 cted with 3x10(5) IU of IL-2 or 0.1 ml of 5% dextrose intraperitoneally every 8 h for 6 d, then kille

185 Controls were pair-fed and received dextrose isocaloric to ethanol.

186 Dextrose isocalorically replaced ethanol in control rats

187 Dextrose isocalorically replaced ethanol in controls.

188 a sugar-based (8.5% w/v sucrose and 0.3% w/v dextrose) isotonic medium.

189 ther placebo (5% dextrose) (n=160), GIK (40% dextrose, K+ 100 mmol.L(-1), insulin 70 u.L(-1)) (0.75 m

190 e-ischemic placebo (5% dextrose) or GIK (40% dextrose, K+ 100 mmol.L(-1), insulin 70 u.L(-1); 0.75 mL

191 age (20 ml/kg of body weight, 0.9% NaCl, 15% dextrose), KO mice had impaired natriuresis (37 +/- 10 v

192 he fasting level (6.1+/-2.73 mmol/l) with 5% dextrose labeled with 6,6[2H2]glucose throughout the AH

193 There was no acid production from dextrose, lactose, maltose, or sucrose.

194 ecognized being hypoglycaemic with the blood dextrose level falling down to 2.2mM or less.

195 %], antibiotic medium 3 [M3], and M3 with 2% dextrose [M3-2%]) and two criteria of MIC determination

196 tion induces partial destruction of Ume6p in dextrose medium and accelerates meiotic degradation by t

197 maintenance of mtDNA in cells grown on rich dextrose medium, but is dispensible in glycerol grown ce

198 nance of mtDNA in rho+ cells growing on rich dextrose medium, we find that it is not required for the

199 g vegetative growth on yeast extract-peptone-dextrose medium.

200 rmal blood cells mixed together in a sucrose/dextrose medium.

201 se, antibiotic medium 3 (M3), and M3 with 2% dextrose, MFCs were determined for each isolate-medium-d

202 Infants were randomized to prophylactic 40% dextrose (n = 681) or placebo (n = 678) gel, 0.5 mL/kg,

203 cruited and randomized to either placebo (5% dextrose) (n=160), GIK (40% dextrose, K+ 100 mmol.L(-1),

204 ibited decreased growth on medium containing dextrose, oleic acid, and cerulenin, an inhibitor of fat

205 TP depletion (5 mM cyanide in the absence of dextrose), on the distribution and function of beta 1 in

206 and Sod1 knockout (Sod1(-/-)) mice were fed dextrose or ethanol (10% of total calories) liquid diets

207 FAT1 deletion strains grown on either dextrose or oleic acid medium accumulated very long-chai

208 l) and (2) continuous infusion of either 50% dextrose or saline (control).

209 llocated to receive pre-ischemic placebo (5% dextrose) or GIK (40% dextrose, K+ 100 mmol.L(-1), insul

210 mol/L of sodium and 5 mmol/L potassium in 5% dextrose) or moderately hypotonic fluid therapy (80 mmol

211 N ranibizumab monotherapy (sham infusion [5% dextrose] PDT and ranibizumab 0.5 mg).

212 iod (9 +/- 38 ppm.h) compared with after the dextrose period (385 +/- 52 ppm.h, P < 0.001).

213 end of the lactose period compared with the dextrose period.

214 ming small colonies on yeast extract/peptone/dextrose plates.

215 Main-trial test meals were dextrose, dextrose plus 10 g lactulose, plain hot rice, or plain c

216 Hypertonic dextrose prolotherapy (DPT) has been reported to be effe

217 -guided Achilles intratendinous hyperosmolar dextrose prolotherapy and introduce a novel, preceding s

218 mM-10mM including the cases of normal blood dextrose range.

219 ystemic caloric contribution of acid-citrate-dextrose regional anticoagulation and dextrose-containin

220 ydrate calories and nutritional support, and dextrose replacement for hypoglycemia prevention and tre

221 and 6 were fed fish oil-ethanol and fish oil-dextrose, respectively, for 8 weeks.

222 dia (standard RPMI-1640 [RPMI], RPMI with 2% dextrose [RPMI-2%], antibiotic medium 3 [M3], and M3 wit

223 tibility of Cryptococcus neoformans using 2% dextrose Sabouraud dextrose agar (SabDex) with fluconazo

224 cterized using surface plasmon resonance for dextrose sensing.

225 parenteral nutrition and those who received dextrose solution (26.0+/-5.4% vs. 26.2+/-5.2%; adjusted

226 ype of anticoagulant used, with acid-citrate-dextrose solution B (ACD-B) providing the best results.

227 mino acid solution (parenteral nutrition) or dextrose solution until full feeding with milk was estab

228 of bimagrumab (10 mg/kg up to 1200 mg in 5% dextrose solution) or placebo (5% dextrose solution) tre

229 0 mg in 5% dextrose solution) or placebo (5% dextrose solution) treatment every 4 weeks for 48 weeks;

230 12.6% ACD/NS solution (anticoagulant citrate dextrose, solution A, USP mixed with 0.9% NaCl, v/v) was

231 signed in a 1:1 manner to the control group (dextrose solutions only) or to the low-glucose intervent

232 and conventional oral diets with intravenous dextrose (standard care), are compared with parenteral n

233 adults were randomly assigned to lactose or dextrose supplementation for 10 d (days 1-10), crossing

234 hese data show that the inhibitory effect of dextrose supplementation on liver regeneration is associ

235 The inhibitory effect of dextrose supplementation on liver regeneration was first

236 Following culture in medium containing dextrose, the added Q(6) was detected in the plasma memb

237 Intravenous fluid and dextrose therapy for illnesses during the first 2 years

238 ed state (i.v. Glamin to double amino acids, dextrose to sustain glucose approximately 7-7.5 mmol l(-

239 intravenous infusion of 12.5 or 25 g of 50% dextrose to the time of (18)F-FDG injection.

240 nerative response to PH was compared between dextrose-treated and control mice.

241 thally injured MPT cells but not to control, dextrose-treated cells, indicating that the beta 1 integ

242 t 50 microg/kg) or vehicle (100 microL of 5% dextrose) treatment was initiated at 1 hr after cecal li

243 A dialysis solution with 2.5% dextrose was administered continuously via one of the ca

244 roxide anion production induced by 500 mg/dl dextrose was inhibited by therapeutic concentrations of

245 Once each minute, 2 mL of cooled 5% dextrose was injected through the pulmonary catheter.

246 Sodium-free 10% dextrose was used as the DSR solution.

247 -480 mins, phenylephrine, normal saline, and dextrose were administered to maintain cerebral perfusio

248 of crystalline mixtures of DZ (20-80 ng) in dextrose were delivered to the medullary reticular forma

249 MGM], Shadomy [SHA], and RPMI 1640 [RPMI, 2% dextrose]) were obtained at 24 to 72 h.

250 to five rats per group) were fed ethanol or dextrose with either corn oil or saturated fat for 1-, 2

251 were switched to isocaloric diets containing dextrose with fish oil (group 2), palm oil (group 3), or

252 ditional group of rats fed either ethanol or dextrose with fish oil or corn oil were supplemented wit

253 media, including Bacto yeast extract-peptone-dextrose (yeast culture medium) broth, Luria-Bertani (ba

254 clinical strain was plated on yeast-peptone-dextrose (YPD) agar with 1 mM CuSO(4), three colony colo