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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 ituitary mediator that appears to act as the counterregulatory hormone for glucocorticoid action with
50   Glucagon is usually viewed as an important counterregulatory hormone in glucose metabolism, with ac
51                                              Counterregulatory hormone levels were collected at each
52 rded middle cerebral artery velocity (VMCA), counterregulatory hormone levels, and cognitive function
53 n response, insulin sensitivity, cytokine or counterregulatory hormone levels, resting energy expendi
54 tion by peripheral tissues, despite systemic counterregulatory hormone release and local sympathetic
55 hin the VMH during hypoglycemia to stimulate counterregulatory hormone release as well.
56  are elevated in diabetes, which may inhibit counterregulatory hormone release during hypoglycemia.
57                      Hypoglycemia stimulates counterregulatory hormone release to restore euglycemia.
58 changes were associated with alternations in counterregulatory hormone release.
59 ts, hypoglycemia was associated with a brisk counterregulatory hormone response (plasma epinephrine 2
60 ddress this question by examining memory and counterregulatory hormone response during hyperglycemia
61 were less pronounced in IAH, indicating that counterregulatory hormone responses are key modulators o
62 he ventromedial hypothalamus (VMH) influence counterregulatory hormone responses during acute hypogly
63 n recipients to assess epinephrine and other counterregulatory hormone responses during hypoglycemia
64 rain to close K(ATP) channels would modulate counterregulatory hormone responses to either brain gluc
65 Local VMH perfusion with L-lactate decreased counterregulatory hormone responses to hypoglycemia by 8
66                                              Counterregulatory hormone responses to hypoglycemia were
67                               In a subgroup, counterregulatory hormone responses to hypoglycemia were
68  and that local VMH glucose perfusion blocks counterregulatory hormone responses.
69  diabetes has been attributed to deficits in counterregulatory hormone secretion.
70        In vivo, dopamine (DA) may serve as a counterregulatory hormone to angiotensin II's acute acti
71 dney, particularly lactate, is stimulated by counterregulatory hormones and accounts for a significan
72 se production by the kidney is stimulated by counterregulatory hormones and represents an important c
73 s, during insulin-induced hypoglycemia, when counterregulatory hormones are absent, liver hypoglycemi
74 pressed as percentage normoxia response) for counterregulatory hormones during hypoglycaemia were sig
75 ing blood glucose and trigger the release of counterregulatory hormones during hypoglycemia.
76 sulin-induced hypoglycemia in the absence of counterregulatory hormones in overnight-fasted conscious
77                 The natriuretic peptides are counterregulatory hormones involved in volume homeostasi
78 ably neuronal activity, precedes the rise in counterregulatory hormones seen during hypoglycemia.
79                           Plasma glucose and counterregulatory hormones were measured during both stu
80     These data indicate that, in addition to counterregulatory hormones, activation of the autonomic
81 rregulatory responses (circulating levels of counterregulatory hormones, intermediary metabolites, su
82  before there was a significant elevation in counterregulatory hormones.
83  hypoglycemia-induced rises in the principal counterregulatory hormones.
84  meal; the pancreas, which produces glycemic counterregulatory hormones; and the brain, which control
85  positively with serum concentrations of the counterregulatory IL-1 receptor antagonist.
86 ed levels of proinflammatory (MIP1gamma) and counterregulatory (IL-12p40, soluble TNFr1/2) factors, b
87 sphorylated beta-receptor domain is a potent counterregulatory inhibitor of the insulin receptor tyro
88 ptosporidiosis mount inflammatory, Th-2, and counterregulatory intestinal immune responses.
89 arly promoted cholesterol efflux, which is a counterregulatory mechanism against foam cell formation.
90 hindlimb ischemia may represent an important counterregulatory mechanism that blunts overactivation o
91 beta signaling is central to an unrecognized counterregulatory mechanism that promotes homeostasis on
92 tes to systemic vasodilation and serves as a counterregulatory mechanism to attenuate pulmonary vasoc
93 increased expression of RGS protein may be a counterregulatory mechanism to inhibit G protein signali
94  with AA, the first potentially indicating a counterregulatory mechanism to suppress cytokines yet no
95 omic nervous system (ANS) and neuroendocrine counterregulatory mechanisms during hypoglycemia.
96 SRI fluoxetine can amplify ANS and metabolic counterregulatory mechanisms during moderate hypoglycemi
97 ppreciation of the role played by endogenous counterregulatory mechanisms in controlling the outcome
98                           To avoid potential counterregulatory mechanisms occurring in constitutive a
99 uced neuroendocrine responses, key metabolic counterregulatory mechanisms of endogenous glucose produ
100           The discovery of several layers of counterregulatory mechanisms reveals how B cells can con
101 cle in heart failure as a result of impaired counterregulatory mechanisms that normally act to attenu
102  d-1mT treatment suggested that compensatory counterregulatory mechanisms were activated by d-1mT, wh
103 es, in the absence of adequate and sustained counterregulatory mechanisms, contribute to pregnancy lo
104  not only for disease induction but also for counterregulatory mechanisms, protecting the heart from
105 han those of JAK2V617F because of at least 2 counterregulatory mechanisms.
106                                          The counterregulatory mediator lipoxin A4 was detectable in
107 nges were accompanied by enhanced adrenergic counterregulatory metabolic responses as well as elevate
108  whereas the soluble receptor functions as a counterregulatory molecule.
109      Cytokines, costimulatory molecules, and counterregulatory molecules control the quality and inte
110                                          Two counterregulatory molecules, TNF-alphaR (TNFR) 1 and TNF
111  the possibility of important prothrombotic, counterregulatory or other sudden cardiac events.
112 therapeutic strategy that emphasizes natural counterregulatory pathways in the airways.
113  macrophage, little is known of the parallel counterregulatory pathways which repress or inhibit macr
114 on, is determined by the net effect of these counterregulatory pathways.
115 sive compensatory vagal activation after the counterregulatory phase may account for bradycardia and
116                                     As such, counterregulatory phosphatases that target mitogen-activ
117 physiologic role of FGF23 may be to act as a counterregulatory phosphaturic hormone to maintain phosp
118 evels, there were significant differences in counterregulatory physiological responses.
119    We propose that the reduced impact of the counterregulatory properties of AnxA1 in CF cells contri
120 rongly suggest that the AT2 receptor plays a counterregulatory protective role mediated via BK and ni
121                                          The counterregulatory response (CRR) to hypoglycemia in vivo
122 ucose is impaired under conditions where the counterregulatory response (CRR) to hypoglycemia is impa
123 5-hydroxytryptamine [5-HT]) in enhancing the counterregulatory response (CRR) to hypoglycemia.
124           This may contribute to the reduced counterregulatory response following repeated bouts of h
125  role of the ANS in mediating this important counterregulatory response in humans remains controversi
126                                The defective counterregulatory response in STZ-diabetic animals was r
127         Hypoglycemia provokes a multifaceted counterregulatory response involving the sympathoadrenal
128 uced hypoglycemia might improve the dampened counterregulatory response seen in tightly controlled di
129 rovide feedback inhibitory regulation of the counterregulatory response through actions within the VM
130 are involved in basal glucoregulation or the counterregulatory response to an insulin-induced decreme
131 ressed, whereas 2-DG infusion amplified, the counterregulatory response to hyperinsulinemic hypoglyce
132 es respond to glucose and play a role in the counterregulatory response to hypoglycaemia in humans.
133  shown the carotid bodies play a role in the counterregulatory response to hypoglycaemia.
134 se is important for proper activation of the counterregulatory response to hypoglycemia and that impa
135 f a catalytic dose of fructose amplifies the counterregulatory response to hypoglycemia by both incre
136 y, insulin acts in the brain to regulate the counterregulatory response to hypoglycemia by directly a
137 t the vagus nerves are not essential for the counterregulatory response to hypoglycemia caused by hig
138               Profound defects in the normal counterregulatory response to hypoglycemia explain the f
139  a paucity of data regarding its role in the counterregulatory response to hypoglycemia in humans.
140 entromedial hypothalamus reduces the glucose counterregulatory response to hypoglycemia in rats (see
141                             Furthermore, the counterregulatory response to hypoglycemia was significa
142 ole in glucose sensing and in regulating the counterregulatory response to hypoglycemia, and if so, w
143 sium channel opener (KCO), NN414, to amplify counterregulatory response to hypoglycemia.
144 rs to play a critical role in initiating the counterregulatory response to hypoglycemia.
145 he vagus nerves is not required for a normal counterregulatory response to hypoglycemia.
146 g neurons in the hypothalamus to mediate the counterregulatory response to hypoglycemia.
147                                Initially the counterregulatory response to identical hypoglycemia was
148 ression of PTX3 found in patients could be a counterregulatory response to injury.
149 GK activity is an important regulator of the counterregulatory response to insulin-induced hypoglycem
150                                          The counterregulatory response to insulin-induced hypoglycem
151                                          The counterregulatory response to insulin-induced hypoglycem
152 6.2/SUR-1-selective KCOs enhance the glucose counterregulatory response to insulin-induced hypoglycem
153 ile decreasing GK activity would enhance the counterregulatory response to insulin-induced hypoglycem
154                          The increase in the counterregulatory response to insulin-induced hypoglycem
155 t of varying hepatic glycogen content on the counterregulatory response to low blood sugar in dogs.
156 lay an important role in the insulin-induced counterregulatory response to mild hypoglycemia.
157                        In protocol 1, a full counterregulatory response was allowed, whereas in proto
158  GK expression are associated with a blunted counterregulatory response, we tested the hypothesis tha
159 ley rats restores the defective hypoglycemia counterregulatory response.
160 e hypoglycemia and initiation of the glucose counterregulatory response.
161 ycemia and initiate part of the compensatory counterregulatory response.
162 ibuted to abnormalities in the blood glucose counterregulatory response.
163                                    Patients' counterregulatory responses (circulating levels of count
164 sodes of hypoglycemia impair sympathoadrenal counterregulatory responses (CRRs) to a subsequent episo
165      Recurrent hypoglycemia impairs hormonal counterregulatory responses (CRRs) to further bouts of h
166 a secondary to impairments in normal glucose counterregulatory responses (CRRs).
167 nct glucosensors to activate sympathoadrenal counterregulatory responses (CRRs).
168 Aergic tone may contribute to suppression of counterregulatory responses after recurrent hypoglycemia
169 uring recurrent hypoglycemia with attenuated counterregulatory responses and comparing it with initia
170                                              Counterregulatory responses and glutamine/glutamate conc
171 ged period after transplantation, we studied counterregulatory responses and symptom recognition in t
172  with type 1 diabetes where both HGR and RGR counterregulatory responses are reduced.
173 ine, autonomic nervous system, and metabolic counterregulatory responses are sensitive to the bluntin
174 within the VMH may modulate the magnitude of counterregulatory responses by altering release of GABA
175  to the impairment in glucagon secretion and counterregulatory responses caused by recurrent hypoglyc
176 amplify a wide spectrum of ANS and metabolic counterregulatory responses during hypoglycemia in healt
177                            The physiology of counterregulatory responses during hypoglycemia in inten
178 ts of fluoxetine on integrated physiological counterregulatory responses during hypoglycemia in type
179 and cardiovascular (systolic blood pressure) counterregulatory responses during hypoglycemia.
180 therapy reduced (P < 0.05) ANS and metabolic counterregulatory responses during hypoglycemia.
181 d, whereas knockdown of VMH ephrinA5 reduced counterregulatory responses during hypoglycemia.
182 e GABA levels sufficiently to fully activate counterregulatory responses during hypoglycemia.
183 autonomic nervous system (ANS) and metabolic counterregulatory responses during next-day hypoglycemia
184 dy was to determine if DHEA-S could preserve counterregulatory responses during repeated hypoglycemia
185 ine, autonomic nervous system, and metabolic counterregulatory responses during subsequent exercise i
186 th the benzodiazepine alprazolam would blunt counterregulatory responses during subsequent exercise,
187  0.05) of neuroendocrine, ANS, and metabolic counterregulatory responses during subsequent hypoglycem
188 cemia preserved neuroendocrine and metabolic counterregulatory responses during subsequent hypoglycem
189 oglycemia preserves autonomic nervous system counterregulatory responses during subsequent hypoglycem
190 nervous system (ANS), metabolic, and symptom counterregulatory responses following hypoglycemia on da
191  studies, the potential for NN414 to restore counterregulatory responses in chronically cannulated no
192              These results demonstrate novel counterregulatory responses in inflammation initiated vi
193 synaptic activity associated with attenuated counterregulatory responses indicates that the dorsal mi
194 fore, interrupting monocyte-mediated vaccine counterregulatory responses may serve as an effective ne
195 perimental and clinical studies suggest that counterregulatory responses mediated by adenosine may be
196           ANS, neuroendocrine, and metabolic counterregulatory responses remained unchanged in the pl
197                                These reduced counterregulatory responses resulted in significantly gr
198                                   Subsequent counterregulatory responses showed marked differences.
199 rmal humans, there is a hierarchy of blunted counterregulatory responses that are determined by the d
200 fferent brain regions sense and modulate the counterregulatory responses that can occur in response t
201 ucose availability stimulate food intake and counterregulatory responses that restore glucose levels
202 ervation of the liver abolished the improved counterregulatory responses that resulted from increased
203  the effects of GABA(A) receptor blockade on counterregulatory responses to a standardized hypoglycem
204 esting euglycemia, patients displayed normal counterregulatory responses to exercise.
205                             We conclude that counterregulatory responses to fixed hypoglycemia differ
206 n the ventromedial hypothalamus mediate some counterregulatory responses to hypoglycemia and 2-deoxyg
207 Currently, physiologic approaches to augment counterregulatory responses to hypoglycemia have not bee
208 ine whether sex-related differences occur in counterregulatory responses to hypoglycemia in adult typ
209  whether knockdown of in the VMH can improve counterregulatory responses to hypoglycemia in diabetic
210 rocess of transplantation per se, we studied counterregulatory responses to hypoglycemia in dogs with
211 euptake inhibitor (SSRI) fluoxetine augments counterregulatory responses to hypoglycemia in healthy h
212 jor role in the sexual dimorphism present in counterregulatory responses to hypoglycemia in healthy h
213 would amplify autonomic nervous system (ANS) counterregulatory responses to hypoglycemia in individua
214 ated sympathoadrenal, symptomatic, and other counterregulatory responses to hypoglycemia on day 2, a
215 BJECTIVE-To determine whether alterations in counterregulatory responses to hypoglycemia through the
216  catecholamine release into the VMH enhances counterregulatory responses to hypoglycemia via stimulat
217 amus (VMH) is crucial for full activation of counterregulatory responses to hypoglycemia, and increas
218 ent hypoglycemia had no effect on subsequent counterregulatory responses to hypoglycemia.
219  within the brain, plays a role in affecting counterregulatory responses to hypoglycemia.
220 cant role in the detection and activation of counterregulatory responses to hypoglycemia.
221 actate raised VMH GABA levels and suppressed counterregulatory responses to hypoglycemia.
222 her blockade of VMH B1AR nor B3AR suppressed counterregulatory responses to hypoglycemia.
223 romedial hypothalamus are thought to mediate counterregulatory responses to hypoglycemia.
224  and adrenal c-fos, consistent with impaired counterregulatory responses to hypoglycemia.
225                              The increase in counterregulatory responses to inflammation in alpha7(-/
226 se production and peripheral glucose uptake) counterregulatory responses to next-day hypoglycemia in
227 in, however, if prior hypoglycemia can blunt counterregulatory responses to other physiologic stresse
228 ts; and 3) antecedent hypoglycemia can blunt counterregulatory responses to other physiologic stresse
229 In nondiabetic subjects, hypoglycemia blunts counterregulatory responses to subsequent exercise.
230 unt autonomic, neuroendocrine, and metabolic counterregulatory responses to subsequent hypoglycemia i
231 ectly on the central nervous system to blunt counterregulatory responses to subsequent hypoglycemia i
232            Antecedent hypoglycemia can blunt counterregulatory responses to subsequent hypoglycemia.
233 erves many critical autonomic nervous system counterregulatory responses to subsequent hypoglycemia;
234 an important role in modulating the hormonal counterregulatory responses triggered by decreases in bl
235 dent responses, including anti-inflammatory, counterregulatory responses via mitogen- and stress-acti
236  neuroendocrine and autonomic nervous system counterregulatory responses was an acute failure of endo
237 tivity, hypoglycemic symptoms, and metabolic counterregulatory responses were equivalent with day 1 r
238 diate glutamate's stimulatory effects on the counterregulatory responses, 3) quantified glutamate met
239                                Subsequently, counterregulatory responses, hypothalamic neuronal activ
240 privation or hypoglycemia induces a range of counterregulatory responses, including glucose mobilizat
241 t hypoglycemia causes blunting of protective counterregulatory responses, known as hypoglycemia-assoc
242            All three treatments restored the counterregulatory responses, suggesting that lactate sup
243                 Repeated hypoglycemia blunts counterregulatory responses, thereby increasing the risk
244 cagon, but not other forms of neuroendocrine counterregulatory responses, to subsequent hypoglycemia.
245  To understand the role of GK in glucoprivic counterregulatory responses, we injected alloxan, a GK i
246  kainic acid receptors in the VMH to augment counterregulatory responses.
247 ory tone within the VMH can modulate glucose counterregulatory responses.
248 ated by 2-deoxyglucose, which also activates counterregulatory responses.
249 blunting of key neuroendocrine and metabolic counterregulatory responses.
250 mia produced specific blunting of subsequent counterregulatory responses.
251 ent autonomic, neuroendocrine, and metabolic counterregulatory responses.
252 could direct pancreatic and hepatic or other counterregulatory responses.
253 n both RH and diabetic rats and restored the counterregulatory responses.
254 urotransmitter may play a role in modulating counterregulatory responses.
255  and therefore might contribute to defective counterregulatory responses.
256 ptide, and muscle sympathetic nerve activity counterregulatory responses.
257 ose kinetics, lipolysis, and glycogenolysis) counterregulatory responses.
258 se findings collectively imply a specialized counterregulatory role for FCRL molecules at the interse
259                   Similar studies revealed a counterregulatory role for IDO during leishmaniasis (res
260 shed by neutrophil depletion, establishing a counterregulatory role for LILRB4 in the absence of mast
261  These results identify a distinct molecular counterregulatory role for spermine in downregulating th
262 -gamma-stimulated p11 expression may serve a counterregulatory role.
263 (LXs) are eicosanoid mediators that play key counterregulatory roles during infection.
264 her, two type 1 cytokines exert dominant and counterregulatory roles: tumor necrosis factor alpha (TN
265 ide evidence for endogenous PD1 as a pivotal counterregulatory signal in allergic airway inflammation
266 mmatory mediators for neutrophils, yet their counterregulatory signaling mechanisms remain to be dete
267 s by activation of a TRIM30alpha-controlled, counterregulatory signaling pathway to protect against e
268             Moreover, they provide potential counterregulatory signals in communication(s) between th
269 itically ill patients is driven by excessive counterregulatory stress hormone release and high tissue
270                           Also activated are counterregulatory systems such as the pituitary-adrenal
271               Our findings establish a novel counterregulatory transmembrane pathway by which mast ce

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