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1 rs in whom there were 1181 episodes of acute hyperammonemia.
2  neuronal disorders that are associated with hyperammonemia.
3 ncy of this enzyme usually results in lethal hyperammonemia.
4 nd punctuated by sometimes fatal episodes of hyperammonemia.
5 ypertension (P = 0.045) were associated with hyperammonemia.
6 e synthetase and consequent life-threatening hyperammonemia.
7 le in development or if it was the result of hyperammonemia.
8 solid organ transplantation be evaluated for hyperammonemia.
9  cycle rate was not significantly altered by hyperammonemia.
10 associated with liver failure and congenital hyperammonemia.
11 ine induced gluconeogenesis and constitutive hyperammonemia.
12 les show an interaction of RhBG-MyD88 during hyperammonemia.
13 ) protected against liver injury and further hyperammonemia.
14 ne, hypercitrullinemia, hyperlactatemia, and hyperammonemia.
15 including hypoglycemia, lactic acidosis, and hyperammonemia.
16 mino acids toward ureagenesis and preventing hyperammonemia.
17 onses during the cellular stress response to hyperammonemia.
18  FLC-associated metabolic changes, including hyperammonemia.
19  causes of acute decompensation with/without hyperammonemia.
20 osylation in myotubes and muscle tissue upon hyperammonemia.
21 e synthesis is a promising strategy to treat hyperammonemia.
22 rapy of both primary and secondary causes of hyperammonemia.
23 en scavenging agents in lung recipients with hyperammonemia.
24 failure patients and to assess its impact on hyperammonemia.
25 or urea synthesis, and deficiency results in hyperammonemia.
26 model with which to study effects of chronic hyperammonemia.
27  myostatin up-regulation under conditions of hyperammonemia.
28 nd in turn, avoid the deleterious effects of hyperammonemia.
29 ion of therapy and the absence of documented hyperammonemia.
30 troencephalogram (EEG) correlates of induced hyperammonemia.
31 t was also tested in a domestic pig model of hyperammonemia.
32 not display the usual neurologic symptoms of hyperammonemia.
33 increased alanine aminotransferase (1%), and hyperammonemia (1%).
34 percent of the patients survived episodes of hyperammonemia (1132 of 1181 episodes).
35 e present the largest case series to date of hyperammonemia after lung transplantation (LTx) and disc
36 f metabolic processes, we determined whether hyperammonemia aggravates ethanol-induced muscle loss.
37 ad orthotopic lung transplantation developed hyperammonemia, all within the first 26 days after trans
38 TLN1 patients and included citrullinemia and hyperammonemia along with delayed cerebellar development
39                                              Hyperammonemia also induced dysregulation of its main me
40 ciduria, an inherited metabolic disease with hyperammonemia and a systemic phenotype coinciding with
41 common urea-cycle disorder, characterized by hyperammonemia and accompanied by a high unmet patient n
42 ry and are potential therapeutic targets for hyperammonemia and chronic liver disease progression.
43                  In patients with cirrhosis, hyperammonemia and hepatic encephalopathy are common aft
44                                 Treatment of hyperammonemia and hepatic encephalopathy in cirrhosis i
45 reagenesis is critical for the prevention of hyperammonemia and hepatic encephalopathy.
46 amine administration may have contributed to hyperammonemia and hyperglutaminemia in this patient.
47 bolism that result in often life-threatening hyperammonemia and hyperglutaminemia.
48         A deficiency of this enzyme leads to hyperammonemia and hyperglutaminemia.
49 patic GS expression in mice causes only mild hyperammonemia and hypoglutaminemia but a pronounced dec
50 tectomy liver failure (PHLF) and ameliorated hyperammonemia and hypoglycemia by providing liver funct
51                               The effects of hyperammonemia and hyponatremia were synergistic.
52                                 The enhanced hyperammonemia and lower fasting blood sugar, which are
53          Although the exact mechanism of how hyperammonemia and LPS facilitate cytotoxic edema and pr
54  vector needed to rescue Nags(-/-) mice from hyperammonemia and measured expression levels of Nags mR
55  inherited metabolic disorders manifested by hyperammonemia and neurological impairment.
56 chronic liver failure are linked to systemic hyperammonemia and often result in cerebral dysfunction
57                     Gene therapy ameliorated hyperammonemia and reduced global methylmalonylation in
58 was to define the individual contribution of hyperammonemia and systemic inflammation on neuroinflamm
59 he mechanisms behind HE are unclear although hyperammonemia and systemic inflammation through gut dys
60 ic encephalopathy (HE) are unclear, although hyperammonemia and systemic inflammation through gut dys
61 c edema because of the synergistic effect of hyperammonemia and the induced inflammatory response.
62  of HE (bile duct ligation [BDL] and induced hyperammonemia) and also evaluated the effect of ammonia
63 th animals exhibiting decreased body weight, hyperammonemia, and brain edema.
64 on and phosphorylation were unaltered during hyperammonemia, and depletion of GSK3beta did not preven
65  (AI) activity, exhibited severe symptoms of hyperammonemia, and died between postnatal days 10 and 1
66 maintained body weight, delayed the onset of hyperammonemia, and reduced brain edema.
67  with episodic rhabdomyolysis, hypoglycemia, hyperammonemia, and susceptibility to life-threatening c
68 e within 36 hours of birth with overwhelming hyperammonemia, and without significant liver pathology.
69 rammonemia in a variety of acute and chronic hyperammonemia animal models, including acute liver fail
70                Failure of the urea cycle and hyperammonemia are common in patients with acute and chr
71 e been reported, but the global responses to hyperammonemia are unclear.
72                                              Hyperammonemia, arising from variety of disorders, leads
73 tamine, reduced myo-inositol and choline are hyperammonemia-associated astrocytic changes, while diff
74 itively) correlated with MR spectroscopy and hyperammonemia-associated astrocytic changes.
75  ammonia and carbon dioxide, contributing to hyperammonemia-associated neurotoxicity and encephalopat
76 Patients with CD develop hepatosteatosis and hyperammonemia but there is no effective therapy for CD.
77 rds regression model clearly showed reducing hyperammonemia by 48 hours after initiating continuous r
78 rmance, systemic inflammation, dysbiosis and hyperammonemia compared to controls and cirrhotics witho
79 nificantly impaired in patients with induced hyperammonemia compared to placebo.
80 ion mortality rate was 67% for patients with hyperammonemia compared with 17% for those without hyper
81                              A case of fatal hyperammonemia complicating orthotopic lung transplantat
82 or longer may represent a useful approach to hyperammonemia control in acute liver failure patients.
83      The recently discovered hyperinsulinism/hyperammonemia disorder showed that the loss of alloster
84 drug approved in Europe for the treatment of hyperammonemia due to PA.
85   Hemodialysis may also be needed to control hyperammonemia, especially in neonates and older patient
86  activity of urea cycle enzymes resulting in hyperammonemia, evidence of hepatic stellate cell activa
87 nstrated that wild-type and hyperinsulinemia/hyperammonemia forms of GDH are inhibited by the green t
88 duced expression of hepatic glucokinase, and hyperammonemia from reduced expression of hepatic carbam
89      In clinically relevant rodent models of hyperammonemia (genetic ornithine transcarbamylase defic
90                                              Hyperammonemia has been associated with intracranial hyp
91          However, pathological studies about hyperammonemia have shown that ammonium is toxic to brai
92            Children with the hyperinsulinism/hyperammonemia (HI/HA) syndrome have symptomatic hypogly
93 his comes from features of the hyperinsulism/hyperammonemia (HI/HA) syndrome where a dominant mutatio
94 cific role in breast cancer, hyperinsulinism/hyperammonemia (HI/HA) syndrome, and neurodegenerative d
95 cid-induced hypoglycemia in hyperinsulinemia hyperammonemia (HI/HA).
96 ase (CPS), as well as dibasic aminoacidurias hyperammonemia-hyperornithinemia-homocitrullinuria (HHH)
97           Their metabolic phenotype includes hyperammonemia, hypoornithinemia, hypocitrullinemia, hyp
98  increased ureagenesis and protected against hyperammonemia in a variety of acute and chronic hyperam
99 ication and is a novel target for therapy of hyperammonemia in both genetic and acquired diseases.
100  a Reye-like syndrome with potentially fatal hyperammonemia in children.
101 nt, persistent, and delayed responses during hyperammonemia in myotubes.
102 ne have been correlated with 'late onset' of hyperammonemia in patients, the effects of these mutatio
103 eficiency, an X-linked trait, leads to toxic hyperammonemia in sparse fur (spf/Y) mice.
104 e condition in the differential diagnosis of hyperammonemia in the neonate and young child.
105  of neurological functions characteristic of hyperammonemia in vivo.
106                           Known responses to hyperammonemia, including mitochondrial and oxidative dy
107 grated these data across different models of hyperammonemia, including myotubes and mouse and human m
108  show that increased liver UDP-GlcNAc during hyperammonemia increases protein O-GlcNAcylation and enh
109 patocyte clones prevented the development of hyperammonemia-induced hepatic encephalopathy.
110 l-shunted rats, they protect recipients from hyperammonemia-induced hepatic encephalopathy.
111 nhibition of RIPK1 and TLR4 protects against hyperammonemia-induced liver injury and are potential th
112       Our work provides unique insights into hyperammonemia-induced myostatin expression and suggests
113         Overexpressing beta-catenin restored hyperammonemia-induced perturbations in signaling respon
114                               In conclusion, hyperammonemia induces liver fibrogenesis and RIPK1-medi
115  Administration-approved oral medication for hyperammonemia, induces astrocytic BDNF and NT-3 express
116                                              Hyperammonemia is a common complication of a wide variet
117                                              Hyperammonemia is a consistent abnormality in cirrhosis
118                                              Hyperammonemia is a consistent abnormality in cirrhosis
119                                              Hyperammonemia is a feature of liver failure, which is a
120                                              Hyperammonemia is a key contributing factor for cerebral
121                                              Hyperammonemia is a major contributing factor to the enc
122                                              Hyperammonemia is a potentially fatal event occurring af
123                                              Hyperammonemia is a rare, often fatal complication after
124                           We postulated that hyperammonemia is an underlying link between hepatic dys
125                                              Hyperammonemia is common in liver cirrhosis and causally
126  early stages of NAFLD, hepatic and systemic hyperammonemia is evident.
127 show that decreased protein synthesis during hyperammonemia is mediated via a novel GSK3beta-independ
128                          The protection from hyperammonemia is reversed by splenectomy.
129 en that elevated plasma arginine rather than hyperammonemia is the major treatment challenge, we prop
130 Unlike other urea cycle disorders, recurrent hyperammonemia is typically less severe in this disorder
131         In this study, we determined whether hyperammonemia leads to hemichannel dysfunction and impa
132            It is now generally accepted that hyperammonemia leads to toxic levels of glutamine in ast
133                              This was due to hyperammonemia, lower phosphorylated AMP-activated prote
134        Kinetic analysis of a hyperinsulinism/hyperammonemia mutant strongly suggests that ATP can inh
135 o (n = 8) or an amino acid solution inducing hyperammonemia (n = 8).
136 atients display acute encephalopathy without hyperammonemia (NonHep E) which is not considered as ove
137                             Life-threatening hyperammonemia occurs in both inherited and acquired liv
138 resented with lethargy, hyperlactatemia, and hyperammonemia of unexplained origin during the neonatal
139 g to diminished protein tolerance and lethal hyperammonemia on a chow diet.
140  demonstrated 100% survival with no signs of hyperammonemia or weight loss to beyond 11 wk, compared
141 mmonemia compared with 17% for those without hyperammonemia (P = 0.01).
142                                       During hyperammonemia, pathways that impact skeletal muscle str
143                                           As hyperammonemia produces cell swelling, we explored the r
144 st early hepatic dysfunction (hyperlactemia, hyperammonemia, prolonged PT time), and normal restituti
145 ppaB kinase beta (IKKbeta) (activated during hyperammonemia), protein interactions, and in vitro kina
146          In vivo studies in mice showed that hyperammonemia reduced muscle mass and strength and incr
147 ildren who were administered carglumic acid, hyperammonemia resolved.
148 atients with cirrhosis, whether induction of hyperammonemia results in neutrophil dysfunction.
149          In this system, we demonstrate that hyperammonemia stimulated myostatin expression in a NF-k
150                                      Because hyperammonemia suggested an enzymatic defect in the allo
151 atty acid oxidation but had no effect on the hyperammonemia suggesting the urea cycle defect was inde
152  of this enzyme that cause a hyperinsulinism-hyperammonemia syndrome (GDH-HI) and sensitize beta-cell
153 ate GTP inhibition cause the hyperinsulinism/hyperammonemia syndrome (HHS), resulting in increased pa
154 lasma species (spp) has been linked to fatal hyperammonemia syndrome (HS) in lung transplant recipien
155                                              Hyperammonemia syndrome (HS) is a rare but potentially f
156 n the patients with sporadic hyperinsulinism-hyperammonemia syndrome and half the normal level in pat
157 his antenna region cause the hyperinsulinism/hyperammonemia syndrome by decreasing GDH sensitivity to
158                             The incidence of hyperammonemia syndrome in LTx patients was approximatel
159                       Patients who developed hyperammonemia syndrome in the posttransplantation perio
160                    The novel hyperinsulinism-hyperammonemia syndrome indicates that GDH-catalyzed glu
161                          The hyperinsulinism-hyperammonemia syndrome is caused by mutations in the gl
162                                              Hyperammonemia syndrome occurred in 5/27 (19%) mollicute
163  of 807 lung transplant recipients developed hyperammonemia syndrome postoperatively during this time
164  underscored by features of hyperinsulinemia/hyperammonemia syndrome, where a dominant mutation cause
165 ic disorder in children, the hyperinsulinism-hyperammonemia syndrome, which is caused by dominantly e
166  unrelated children with the hyperinsulinism-hyperammonemia syndrome: six with sporadic cases and two
167 s not enter hepatocytes and does not improve hyperammonemia that accounts for lethality.
168                                        Under hyperammonemia the observed increase in glutamine synthe
169                                        Under hyperammonemia the value of V(TCA) was 0.57 +/- 0.16 mic
170  and function and molecular perturbations of hyperammonemia; these preclinical studies complement pre
171    Hepatic autophagy is triggered in vivo by hyperammonemia through an alpha-ketoglutarate-dependent
172 t is concluded that TauT deficiency triggers hyperammonemia through impaired hepatic glutamine synthe
173                                              Hyperammonemia triggered activation of IkappaB kinase, N
174 pite multiple therapeutic interventions, the hyperammonemia ultimately resulted in the patient's deat
175 e measured rate of glutamine synthesis under hyperammonemia was 0.43 +/- 0.14 micromol/min per g (mea
176           In a large cohort of ALF patients, hyperammonemia was associated with high-grade HE and wor
177 ed that this syndrome of hyperinsulinism and hyperammonemia was caused by excessive activity of gluta
178                                              Hyperammonemia was defined by NH3 >50 umol/L.
179 insulinism characterized by hypoglycemia and hyperammonemia was described recently.
180                                              Hyperammonemia was even greater as well.
181                                Surprisingly, hyperammonemia was present at an age of 3 and 12 months
182 nd Ass(+/-) mice (Ass(-/-) are lethal due to hyperammonemia) were exposed to an ethanol binge or to c
183                                       During hyperammonemia, when hepatic metabolism is impaired, non
184 t appear normal at birth but rapidly develop hyperammonemia, which can progress to cerebral edema, co
185 (-/-)) mouse is an animal model of inducible hyperammonemia, which develops hyperammonemia without N-
186 dy suggest that hepatic steatosis results in hyperammonemia, which is associated with progression of
187                                 We show that hyperammonemia, which occurs in diverse chronic disorder
188    Hepatic deletion of GS triggered systemic hyperammonemia, which was associated with cerebral oxida
189  and increased autophagy flux in response to hyperammonemia, which were partially reversed following
190  of inducible hyperammonemia, which develops hyperammonemia without N-carbamylglutamate and L-citrull
191                  In a mouse model of chronic hyperammonemia without preexisting liver disease, we obs

 
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