ライフサイエンスコーパス: counterregulatory

1 xaenoic acid in human asthma in vivo and PD1 counterregulatory actions in allergic airway inflammatio

2 Less well studied are the counterregulatory actions of glucagon on protein metabol

3 The counterregulatory actions of insulin on catecholamine ac

4 RvE1 possesses a unique structure and counterregulatory actions that stop human polymorphonucl

5 with other receptors (e.g., ChemR23-mediated counterregulatory actions) to mediate the resolution of

6 This induces inappropriate counterregulatory alterations in fat oxidation during en

7 utely ill patients owing to a combination of counterregulatory and stress responses, as well as insul

8 IL-6 may be an important anti-inflammatory, counterregulatory, and healing cytokine in the airway.

9 We conclude that there is a liver-brain counterregulatory axis that is responsive to liver glyco

10 2 effector CD4+ T cells orchestrate distinct counterregulatory biological responses.

11 -lipoxin receptor (FPR2/ALXR), LXA4, and its counterregulatory compound, leukotriene B4 (LTB4), in pa

12 nopathology is through the production of the counterregulatory cytokine gamma interferon (IFN-gamma),

13 The counterregulatory cytokine IL-10 was exclusively elevate

14 ha) and interleukin-8 (IL-8) relative to the counterregulatory cytokine IL-6 during the first week of

15 oduction of interleukin (IL)-12, a major Th2 counterregulatory cytokine.

16 a second infection by blocking expression of counterregulatory cytokines (IL-6 and IL-10), predisposi

17 athogen P. gingivalis, leading to release of counterregulatory cytokines and the formation of T cell-

18 to village, and increased production of the counterregulatory cytokines IL-10 or TGF-beta by PBMC di

19 ediate DC activation/maturation, but also of counterregulatory cytokines that may prevent a Th-polari

20 kely that the increase in VIF may serve as a counterregulatory effect to defend against hypertension.

21 These studies capitalize on the complex counterregulatory effects of Th1 and Th2 cytokines in vi

22 acting factors that are involved in exerting counterregulatory effects on ASBT mRNA stability.

23 Targeting Hsp90 is typically limited by counterregulatory elevation of Hsp70B, which induces res

24 de or 2.7 microg/min tolbutamide) suppressed counterregulatory (epinephrine and glucagon) responses t

25 ing long-term agonist exposure, indicating a counterregulatory event.

26 lycemia of 2.9 mmol/l produced similar day 2 counterregulatory failure as day 1 hypoglycemia of 3.3 m

27 Thus, counterregulatory failure could be due to relatively enh

28 cemia, in type 1 diabetes, can produce acute counterregulatory failure during a subsequent episode of

29 hat prior hypoglycemia could result in acute counterregulatory failure during subsequent exercise in

30 nd 2) antecedent hypoglycemia will result in counterregulatory failure during subsequent hypoglycemia

31 ine, autonomic nervous system, and metabolic counterregulatory failure during subsequent submaximal e

32 inobutyric acid (GABA) output contributes to counterregulatory failure in recurrently hypoglycemic (R

33 Lactate likely contributes to counterregulatory failure in RH and diabetes by increasi

34 role in the development of exercise-related counterregulatory failure in those with type 1 diabetes.

35 ponse to hypoglycemia and the development of counterregulatory failure in type 1 diabetes.

36 mia of only 3.3 +/- 0.1 mmol/l can result in counterregulatory failure in type 2 diabetic patients wi

37 These data indicate that counterregulatory failure may be a significant in vivo m

38 s in glucose-inhibited neurons might reverse counterregulatory failure.

39 ycemia regulates the magnitude of subsequent counterregulatory failure.

40 synthetic pathways with RH may contribute to counterregulatory failure.

41 ponsible for causing subsequent hypoglycemic counterregulatory failure; and (c) our results suggest t

42 ure can be regulated by the interaction of 2 counterregulatory GPCRs.

43 conclusion, our results demonstrate that the counterregulatory HO-1/CO pathway, which is critical in

44 ge of key neuroendocrine, ANS, and metabolic counterregulatory homeostatic responses during repeated

45 halamic activation and the initiation of the counterregulatory hormonal response to small decrements

46 ycemia symptom scores were recorded, and the counterregulatory hormonal response was measured.

47 We measured plasma counterregulatory hormonal responses and whole-brain CMR

48 c clamps (nadir 60 mg/dL) with evaluation of counterregulatory hormonal responses, endogenous glucose

49 Both surgical injury with HS and counterregulatory hormone (epinephrine) infusion profoun

50 cemic clamp, SGLT2 inhibition did not change counterregulatory hormone concentrations, time to recove

51 ituitary mediator that appears to act as the counterregulatory hormone for glucocorticoid action with

52 Glucagon is usually viewed as an important counterregulatory hormone in glucose metabolism, with ac

53 Counterregulatory hormone levels were collected at each

54 rded middle cerebral artery velocity (VMCA), counterregulatory hormone levels, and cognitive function

55 n response, insulin sensitivity, cytokine or counterregulatory hormone levels, resting energy expendi

56 tion by peripheral tissues, despite systemic counterregulatory hormone release and local sympathetic

57 hin the VMH during hypoglycemia to stimulate counterregulatory hormone release as well.

58 are elevated in diabetes, which may inhibit counterregulatory hormone release during hypoglycemia.

59 Hypoglycemia stimulates counterregulatory hormone release to restore euglycemia.

60 changes were associated with alternations in counterregulatory hormone release.

61 ts, hypoglycemia was associated with a brisk counterregulatory hormone response (plasma epinephrine 2

62 ddress this question by examining memory and counterregulatory hormone response during hyperglycemia

63 suppression in the VMN had no impact on the counterregulatory hormone response to hypoglycemia or on

64 were less pronounced in IAH, indicating that counterregulatory hormone responses are key modulators o

65 he ventromedial hypothalamus (VMH) influence counterregulatory hormone responses during acute hypogly

66 n recipients to assess epinephrine and other counterregulatory hormone responses during hypoglycemia

67 rain to close K(ATP) channels would modulate counterregulatory hormone responses to either brain gluc

68 Local VMH perfusion with L-lactate decreased counterregulatory hormone responses to hypoglycemia by 8

69 Counterregulatory hormone responses to hypoglycemia were

70 In a subgroup, counterregulatory hormone responses to hypoglycemia were

71 and that local VMH glucose perfusion blocks counterregulatory hormone responses.

72 diabetes has been attributed to deficits in counterregulatory hormone secretion.

73 Astrocyte GLUT2 controls glucose counterregulatory hormone secretion.

74 Glucagon is classically described as a counterregulatory hormone that plays an essential role i

75 In vivo, dopamine (DA) may serve as a counterregulatory hormone to angiotensin II's acute acti

76 Glucagon is historically described as the counterregulatory hormone to insulin, induced by fasting

77 dney, particularly lactate, is stimulated by counterregulatory hormones and accounts for a significan

78 During hypoglycemia, attenuated responses of counterregulatory hormones and improvements in cognitive

79 se production by the kidney is stimulated by counterregulatory hormones and represents an important c

80 s, during insulin-induced hypoglycemia, when counterregulatory hormones are absent, liver hypoglycemi

81 pressed as percentage normoxia response) for counterregulatory hormones during hypoglycaemia were sig

82 ing blood glucose and trigger the release of counterregulatory hormones during hypoglycemia.

83 sulin-induced hypoglycemia in the absence of counterregulatory hormones in overnight-fasted conscious

84 The natriuretic peptides are counterregulatory hormones involved in volume homeostasi

85 ably neuronal activity, precedes the rise in counterregulatory hormones seen during hypoglycemia.

86 neuroendocrine system increases secretion of counterregulatory hormones that promote rapid mobilizati

87 Plasma glucose and counterregulatory hormones were measured during both stu

88 These data indicate that, in addition to counterregulatory hormones, activation of the autonomic

89 rregulatory responses (circulating levels of counterregulatory hormones, intermediary metabolites, su

90 before there was a significant elevation in counterregulatory hormones.

91 hypoglycemia-induced rises in the principal counterregulatory hormones.

92 meal; the pancreas, which produces glycemic counterregulatory hormones; and the brain, which control

93 positively with serum concentrations of the counterregulatory IL-1 receptor antagonist.

94 ed levels of proinflammatory (MIP1gamma) and counterregulatory (IL-12p40, soluble TNFr1/2) factors, b

95 sphorylated beta-receptor domain is a potent counterregulatory inhibitor of the insulin receptor tyro

96 ptosporidiosis mount inflammatory, Th-2, and counterregulatory intestinal immune responses.

97 arly promoted cholesterol efflux, which is a counterregulatory mechanism against foam cell formation.

98 This counterregulatory mechanism is impaired in diabetes.

99 hindlimb ischemia may represent an important counterregulatory mechanism that blunts overactivation o

100 beta signaling is central to an unrecognized counterregulatory mechanism that promotes homeostasis on

101 tes to systemic vasodilation and serves as a counterregulatory mechanism to attenuate pulmonary vasoc

102 increased expression of RGS protein may be a counterregulatory mechanism to inhibit G protein signali

103 with AA, the first potentially indicating a counterregulatory mechanism to suppress cytokines yet no

104 omic nervous system (ANS) and neuroendocrine counterregulatory mechanisms during hypoglycemia.

105 SRI fluoxetine can amplify ANS and metabolic counterregulatory mechanisms during moderate hypoglycemi

106 ppreciation of the role played by endogenous counterregulatory mechanisms in controlling the outcome

107 To avoid potential counterregulatory mechanisms occurring in constitutive a

108 uced neuroendocrine responses, key metabolic counterregulatory mechanisms of endogenous glucose produ

109 The discovery of several layers of counterregulatory mechanisms reveals how B cells can con

110 cle in heart failure as a result of impaired counterregulatory mechanisms that normally act to attenu

111 d-1mT treatment suggested that compensatory counterregulatory mechanisms were activated by d-1mT, wh

112 es, in the absence of adequate and sustained counterregulatory mechanisms, contribute to pregnancy lo

113 not only for disease induction but also for counterregulatory mechanisms, protecting the heart from

114 han those of JAK2V617F because of at least 2 counterregulatory mechanisms.

115 The counterregulatory mediator lipoxin A4 was detectable in

116 nges were accompanied by enhanced adrenergic counterregulatory metabolic responses as well as elevate

117 whereas the soluble receptor functions as a counterregulatory molecule.

118 Cytokines, costimulatory molecules, and counterregulatory molecules control the quality and inte

119 Two counterregulatory molecules, TNF-alphaR (TNFR) 1 and TNF

120 the possibility of important prothrombotic, counterregulatory or other sudden cardiac events.

121 therapeutic strategy that emphasizes natural counterregulatory pathways in the airways.

122 macrophage, little is known of the parallel counterregulatory pathways which repress or inhibit macr

123 on, is determined by the net effect of these counterregulatory pathways.

124 sive compensatory vagal activation after the counterregulatory phase may account for bradycardia and

125 As such, counterregulatory phosphatases that target mitogen-activ

126 physiologic role of FGF23 may be to act as a counterregulatory phosphaturic hormone to maintain phosp

127 evels, there were significant differences in counterregulatory physiological responses.

128 We propose that the reduced impact of the counterregulatory properties of AnxA1 in CF cells contri

129 rongly suggest that the AT2 receptor plays a counterregulatory protective role mediated via BK and ni

130 Components of the counterregulatory response (CRR) system that help minimi

131 The counterregulatory response (CRR) to hypoglycemia in vivo

132 ucose is impaired under conditions where the counterregulatory response (CRR) to hypoglycemia is impa

133 5-hydroxytryptamine [5-HT]) in enhancing the counterregulatory response (CRR) to hypoglycemia.

134 tration of miglitol effectively restored the counterregulatory response following antecedent hypoglyc

135 This may contribute to the reduced counterregulatory response following repeated bouts of h

136 role of the ANS in mediating this important counterregulatory response in humans remains controversi

137 The defective counterregulatory response in STZ-diabetic animals was r

138 Hypoglycemia provokes a multifaceted counterregulatory response involving the sympathoadrenal

139 uced hypoglycemia might improve the dampened counterregulatory response seen in tightly controlled di

140 rovide feedback inhibitory regulation of the counterregulatory response through actions within the VM

141 are involved in basal glucoregulation or the counterregulatory response to an insulin-induced decreme

142 ressed, whereas 2-DG infusion amplified, the counterregulatory response to hyperinsulinemic hypoglyce

143 es respond to glucose and play a role in the counterregulatory response to hypoglycaemia in humans.

144 shown the carotid bodies play a role in the counterregulatory response to hypoglycaemia.

145 se is important for proper activation of the counterregulatory response to hypoglycemia and that impa

146 f a catalytic dose of fructose amplifies the counterregulatory response to hypoglycemia by both incre

147 y, insulin acts in the brain to regulate the counterregulatory response to hypoglycemia by directly a

148 t the vagus nerves are not essential for the counterregulatory response to hypoglycemia caused by hig

149 Profound defects in the normal counterregulatory response to hypoglycemia explain the f

150 a paucity of data regarding its role in the counterregulatory response to hypoglycemia in humans.

151 entromedial hypothalamus reduces the glucose counterregulatory response to hypoglycemia in rats (see

152 Furthermore, the counterregulatory response to hypoglycemia was significa

153 ole in glucose sensing and in regulating the counterregulatory response to hypoglycemia, and if so, w

154 g neurons in the hypothalamus to mediate the counterregulatory response to hypoglycemia.

155 of the hypothalamus (VMN) is involved in the counterregulatory response to hypoglycemia.

156 MN GI neurons is not required for the normal counterregulatory response to hypoglycemia.

157 sium channel opener (KCO), NN414, to amplify counterregulatory response to hypoglycemia.

158 rs to play a critical role in initiating the counterregulatory response to hypoglycemia.

159 he vagus nerves is not required for a normal counterregulatory response to hypoglycemia.

160 e identified may play a critical role in the counterregulatory response to hypoglycemia.

161 Initially the counterregulatory response to identical hypoglycemia was

162 ression of PTX3 found in patients could be a counterregulatory response to injury.

163 GK activity is an important regulator of the counterregulatory response to insulin-induced hypoglycem

164 The counterregulatory response to insulin-induced hypoglycem

165 The counterregulatory response to insulin-induced hypoglycem

166 6.2/SUR-1-selective KCOs enhance the glucose counterregulatory response to insulin-induced hypoglycem

167 ile decreasing GK activity would enhance the counterregulatory response to insulin-induced hypoglycem

168 Silencing VMNCCKBR neurons also impaired the counterregulatory response to insulin-induced hypoglycem

169 The increase in the counterregulatory response to insulin-induced hypoglycem

170 t of varying hepatic glycogen content on the counterregulatory response to low blood sugar in dogs.

171 lay an important role in the insulin-induced counterregulatory response to mild hypoglycemia.

172 In protocol 1, a full counterregulatory response was allowed, whereas in proto

173 ration of insulin due to an impaired glucose counterregulatory response, as evidenced by reduced hepa

174 GK expression are associated with a blunted counterregulatory response, we tested the hypothesis tha

175 e hypoglycemia and initiation of the glucose counterregulatory response.

176 ycemia and initiate part of the compensatory counterregulatory response.

177 ibuted to abnormalities in the blood glucose counterregulatory response.

178 ley rats restores the defective hypoglycemia counterregulatory response.

179 Patients' counterregulatory responses (circulating levels of count

180 sodes of hypoglycemia impair sympathoadrenal counterregulatory responses (CRRs) to a subsequent episo

181 Recurrent hypoglycemia impairs hormonal counterregulatory responses (CRRs) to further bouts of h

182 are essential for elicitation of protective counterregulatory responses (CRRs) to glucose deficit, i

183 a secondary to impairments in normal glucose counterregulatory responses (CRRs).

184 nct glucosensors to activate sympathoadrenal counterregulatory responses (CRRs).

185 Aergic tone may contribute to suppression of counterregulatory responses after recurrent hypoglycemia

186 uring recurrent hypoglycemia with attenuated counterregulatory responses and comparing it with initia

187 Counterregulatory responses and glutamine/glutamate conc

188 ged period after transplantation, we studied counterregulatory responses and symptom recognition in t

189 with type 1 diabetes where both HGR and RGR counterregulatory responses are reduced.

190 ine, autonomic nervous system, and metabolic counterregulatory responses are sensitive to the bluntin

191 within the VMH may modulate the magnitude of counterregulatory responses by altering release of GABA

192 to the impairment in glucagon secretion and counterregulatory responses caused by recurrent hypoglyc

193 amplify a wide spectrum of ANS and metabolic counterregulatory responses during hypoglycemia in healt

194 The physiology of counterregulatory responses during hypoglycemia in inten

195 ts of fluoxetine on integrated physiological counterregulatory responses during hypoglycemia in type

196 and cardiovascular (systolic blood pressure) counterregulatory responses during hypoglycemia.

197 therapy reduced (P < 0.05) ANS and metabolic counterregulatory responses during hypoglycemia.

198 d, whereas knockdown of VMH ephrinA5 reduced counterregulatory responses during hypoglycemia.

199 e GABA levels sufficiently to fully activate counterregulatory responses during hypoglycemia.

200 autonomic nervous system (ANS) and metabolic counterregulatory responses during next-day hypoglycemia

201 dy was to determine if DHEA-S could preserve counterregulatory responses during repeated hypoglycemia

202 ine, autonomic nervous system, and metabolic counterregulatory responses during subsequent exercise i

203 th the benzodiazepine alprazolam would blunt counterregulatory responses during subsequent exercise,

204 0.05) of neuroendocrine, ANS, and metabolic counterregulatory responses during subsequent hypoglycem

205 cemia preserved neuroendocrine and metabolic counterregulatory responses during subsequent hypoglycem

206 oglycemia preserves autonomic nervous system counterregulatory responses during subsequent hypoglycem

207 nervous system (ANS), metabolic, and symptom counterregulatory responses following hypoglycemia on da

208 sulinemic-euglycemic (EU) clamp, and glucose counterregulatory responses from a subsequent hypoglycem

209 studies, the potential for NN414 to restore counterregulatory responses in chronically cannulated no

210 These results demonstrate novel counterregulatory responses in inflammation initiated vi

211 synaptic activity associated with attenuated counterregulatory responses indicates that the dorsal mi

212 on-induced feeding while leaving other major counterregulatory responses intact.

213 fore, interrupting monocyte-mediated vaccine counterregulatory responses may serve as an effective ne

214 perimental and clinical studies suggest that counterregulatory responses mediated by adenosine may be

215 ANS, neuroendocrine, and metabolic counterregulatory responses remained unchanged in the pl

216 These reduced counterregulatory responses resulted in significantly gr

217 Subsequent counterregulatory responses showed marked differences.

218 rmal humans, there is a hierarchy of blunted counterregulatory responses that are determined by the d

219 fferent brain regions sense and modulate the counterregulatory responses that can occur in response t

220 ucose availability stimulate food intake and counterregulatory responses that restore glucose levels

221 ervation of the liver abolished the improved counterregulatory responses that resulted from increased

222 the effects of GABA(A) receptor blockade on counterregulatory responses to a standardized hypoglycem

223 esting euglycemia, patients displayed normal counterregulatory responses to exercise.

224 We conclude that counterregulatory responses to fixed hypoglycemia differ

225 n the ventromedial hypothalamus mediate some counterregulatory responses to hypoglycemia and 2-deoxyg

226 Counterregulatory responses to hypoglycemia during a hyp

227 Currently, physiologic approaches to augment counterregulatory responses to hypoglycemia have not bee

228 ine whether sex-related differences occur in counterregulatory responses to hypoglycemia in adult typ

229 whether knockdown of in the VMH can improve counterregulatory responses to hypoglycemia in diabetic

230 rocess of transplantation per se, we studied counterregulatory responses to hypoglycemia in dogs with

231 euptake inhibitor (SSRI) fluoxetine augments counterregulatory responses to hypoglycemia in healthy h

232 jor role in the sexual dimorphism present in counterregulatory responses to hypoglycemia in healthy h

233 would amplify autonomic nervous system (ANS) counterregulatory responses to hypoglycemia in individua

234 PR119 with MBX-2982 did not improve glucagon counterregulatory responses to hypoglycemia in participa

235 nd pancreatic islet cells, augments glucagon counterregulatory responses to hypoglycemia in preclinic

236 pha-cell GPR119 receptors increases glucagon counterregulatory responses to hypoglycemia in preclinic

237 ated sympathoadrenal, symptomatic, and other counterregulatory responses to hypoglycemia on day 2, a

238 BJECTIVE-To determine whether alterations in counterregulatory responses to hypoglycemia through the

239 catecholamine release into the VMH enhances counterregulatory responses to hypoglycemia via stimulat

240 amus (VMH) is crucial for full activation of counterregulatory responses to hypoglycemia, and increas

241 romedial hypothalamus are thought to mediate counterregulatory responses to hypoglycemia.

242 and adrenal c-fos, consistent with impaired counterregulatory responses to hypoglycemia.

243 ent hypoglycemia had no effect on subsequent counterregulatory responses to hypoglycemia.

244 within the brain, plays a role in affecting counterregulatory responses to hypoglycemia.

245 cant role in the detection and activation of counterregulatory responses to hypoglycemia.

246 actate raised VMH GABA levels and suppressed counterregulatory responses to hypoglycemia.

247 her blockade of VMH B1AR nor B3AR suppressed counterregulatory responses to hypoglycemia.

248 The increase in counterregulatory responses to inflammation in alpha7(-/

249 T1D); however, little is known about how the counterregulatory responses to low blood sugar are affec

250 se production and peripheral glucose uptake) counterregulatory responses to next-day hypoglycemia in

251 in, however, if prior hypoglycemia can blunt counterregulatory responses to other physiologic stresse

252 ts; and 3) antecedent hypoglycemia can blunt counterregulatory responses to other physiologic stresse

253 In nondiabetic subjects, hypoglycemia blunts counterregulatory responses to subsequent exercise.

254 unt autonomic, neuroendocrine, and metabolic counterregulatory responses to subsequent hypoglycemia i

255 ectly on the central nervous system to blunt counterregulatory responses to subsequent hypoglycemia i

256 Antecedent hypoglycemia can blunt counterregulatory responses to subsequent hypoglycemia.

257 erves many critical autonomic nervous system counterregulatory responses to subsequent hypoglycemia;

258 Antecedent hypoglycemia suppresses the counterregulatory responses to subsequent hypoglycemic e

259 an important role in modulating the hormonal counterregulatory responses triggered by decreases in bl

260 dent responses, including anti-inflammatory, counterregulatory responses via mitogen- and stress-acti

261 neuroendocrine and autonomic nervous system counterregulatory responses was an acute failure of endo

262 tivity, hypoglycemic symptoms, and metabolic counterregulatory responses were equivalent with day 1 r

263 diate glutamate's stimulatory effects on the counterregulatory responses, 3) quantified glutamate met

264 Subsequently, counterregulatory responses, hypothalamic neuronal activ

265 privation or hypoglycemia induces a range of counterregulatory responses, including glucose mobilizat

266 t hypoglycemia causes blunting of protective counterregulatory responses, known as hypoglycemia-assoc

267 Among these so-called counterregulatory responses, secretion of glucagon from

268 All three treatments restored the counterregulatory responses, suggesting that lactate sup

269 Repeated hypoglycemia blunts counterregulatory responses, thereby increasing the risk

270 cagon, but not other forms of neuroendocrine counterregulatory responses, to subsequent hypoglycemia.

271 To understand the role of GK in glucoprivic counterregulatory responses, we injected alloxan, a GK i

272 ose kinetics, lipolysis, and glycogenolysis) counterregulatory responses.

273 ory tone within the VMH can modulate glucose counterregulatory responses.

274 kainic acid receptors in the VMH to augment counterregulatory responses.

275 ated by 2-deoxyglucose, which also activates counterregulatory responses.

276 blunting of key neuroendocrine and metabolic counterregulatory responses.

277 mia produced specific blunting of subsequent counterregulatory responses.

278 ent autonomic, neuroendocrine, and metabolic counterregulatory responses.

279 could direct pancreatic and hepatic or other counterregulatory responses.

280 n both RH and diabetic rats and restored the counterregulatory responses.

281 urotransmitter may play a role in modulating counterregulatory responses.

282 and therefore might contribute to defective counterregulatory responses.

283 ptide, and muscle sympathetic nerve activity counterregulatory responses.

284 se findings collectively imply a specialized counterregulatory role for FCRL molecules at the interse

285 Similar studies revealed a counterregulatory role for IDO during leishmaniasis (res

286 shed by neutrophil depletion, establishing a counterregulatory role for LILRB4 in the absence of mast

287 ves glucose homeostasis in vivo, revealing a counterregulatory role for PGC1A in repressing uncontrol

288 These results identify a distinct molecular counterregulatory role for spermine in downregulating th

289 P1) is known to induce PD-L1/L2, a potential counterregulatory role of EBV miR in the fine-tuning of

290 EBV miR-BHRF1-2-5p plays a context-dependent counterregulatory role to fine-tune the expression of th

291 -gamma-stimulated p11 expression may serve a counterregulatory role.

292 (LXs) are eicosanoid mediators that play key counterregulatory roles during infection.

293 her, two type 1 cytokines exert dominant and counterregulatory roles: tumor necrosis factor alpha (TN

294 ide evidence for endogenous PD1 as a pivotal counterregulatory signal in allergic airway inflammation

295 mmatory mediators for neutrophils, yet their counterregulatory signaling mechanisms remain to be dete

296 s by activation of a TRIM30alpha-controlled, counterregulatory signaling pathway to protect against e

297 Moreover, they provide potential counterregulatory signals in communication(s) between th

298 itically ill patients is driven by excessive counterregulatory stress hormone release and high tissue

299 Also activated are counterregulatory systems such as the pituitary-adrenal

300 Our findings establish a novel counterregulatory transmembrane pathway by which mast ce