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1 serum ferritin (a traditional marker of iron overload).
2 or FPN responsiveness to HAMP result in iron overload.
3 eat diseases related to mitochondrial Ca(2+) overload.
4  constriction as a model of cardiac pressure overload.
5 s during hypokalemia, associated with Ca(2+) overload.
6 -rich secretory proteins, thus preventing ER overload.
7 nd improved systolic function after pressure overload.
8 ysate sodium with the goal of reducing fluid overload.
9 IE), anemia, splenomegaly, and systemic iron overload.
10 n (LPO) and steatosis in the absence of iron overload.
11 rease in misfolded SOD1 burden and autophagy overload.
12 e erythroblasts that was independent of iron overload.
13  under the cardiac stress caused by pressure overload.
14 delines for populations "at risk" for volume overload.
15 way is perturbed in diseases that cause iron overload.
16  translational level in response to pressure overload.
17 c remodeling in response to chronic pressure overload.
18 sphorylation in cardiac response to pressure overload.
19 ake, cytoskeleton disruption, or cholesterol overload.
20 -2alpha in iron deficiency, anemia, and iron overload.
21 esponse to systemic iron deficiency and iron overload.
22 bound, pol II-regulated genes after pressure overload.
23 liver iron concentration and myocardial iron overload.
24 anemia and its complications, including iron overload.
25 cell survival under the condition of an iron overload.
26 tion is significantly lowered during calcium overload.
27 toxic iron from patients with secondary iron overload.
28  the consequences of low to moderate calcium overload.
29 al posttranslational control to prevent iron overload.
30 and how this is corrupted by lipid lysosomal overload.
31 ale digesters exposed to a transient organic overload.
32 mediated cardiac protection against pressure overload.
33 hat the exercise order interferes in cardiac overload.
34 osis in mice subjected to sustained pressure overload.
35 by transaortic constriction-induced pressure overload.
36 rts of mice subjected to chronic hemodynamic overload.
37 ons, but without clinical evidence of volume overload.
38 l cardiac remodeling in response to pressure overload.
39 y the diffuse local inflammation in pressure overload.
40 ory leukocyte infiltration early in pressure overload.
41  erythroblast populations regardless of iron overload.
42 he severity of which is related to porphyrin overload.
43 lt and water, contributing to further volume overload.
44 thological LV remodelling following pressure overload.
45 ntestinal iron absorption and therefore iron Overload.
46 les and protect mutant cells from acute iron overload.
47 ed as a compensatory mechanism for metabolic overload.
48 sting a counteracting effect to avoid Ca(2+) overload.
49 Mcub(-/-) mice were more sensitive to Ca(2+) overload.
50 sufficiency causing right ventricular volume overload.
51 rtant when mitochondrial FAO is defective or overloaded.
52 al YKL-40 increased in experimental pressure overload (6-fold in decompensated versus sham mice).
53              Under conditions of cholesterol overload, ACAT1 maintains the low cholesterol concentrat
54 rogram and disrupts the response to pressure overload, accompanied by prominent effects on metabolism
55 d the muscle damage, suggesting that calcium overload acts as one of the early triggers and activates
56                However, mitochondrial Ca(2+) overload also directly causes mitochondrial rupture and
57                  In order to avoid metabolic overload, an emerging area of focus is on engineering co
58 es are more closely associated with hospital overload and are earlier markers of the spread of infect
59 n exporter in mammals, leading to organ iron overload and associated morbidities.
60                                        Fluid overload and cumulative fluid balance were both associat
61 gic cues underlies genetic disorders of iron overload and deficiency, including hereditary hemochroma
62      Mitochondrial dysfunction causes Ca(2+) overload and ECM degradation-mediated muscle damage in C
63 H(2) O(2) during ageing by preventing Ca(2+) overload and endothelial integrity promotes SMC survival
64  represents a potential therapy for glycogen overload and hepatosteatosis associated with GSD Ia, wit
65 (BA) induces a profound mitochondrial Ca(2+) overload and impaired uncoupled respiration.
66 ls subjected to hypokalemia exhibited Ca(2+) overload and increased generation of both spontaneous Ca
67 ulation of CRT results in mitochondrial Ca2+ overload and induction of mitochondria permeability tran
68 halassemia (TDT) mainly chronic anemia, iron overload and iron chelator toxicity.
69 matrix are poised to mitigate beta-oxidation overload and maintain CoA availability.
70    We examined the association between fluid overload and major adverse kidney events in critically i
71 alcium homeostasis to prevent excess calcium overload and mitochondrial dysfunction.
72 viewed and synthesized the evidence on fluid overload and mortality in critically ill patients and ha
73 e targets to intercept mitochondrial calcium overload and necrosis of mycobacterium-infected zebrafis
74  adjusted risk estimates suggests that fluid overload and positive cumulative fluid balance are assoc
75  of matrix Acots can mitigate beta-oxidation overload and prevent CoA limitation.
76 e excitotoxicity by reduction of the calcium overload and restoration of mitochondrial function.SIGNI
77 ts in chronic left ventricular (LV) pressure overload and subsequently leads to LV diastolic dysfunct
78 wledge of transfusion-associated circulatory overload and the safety of transfusion in ICU patients.
79 bly involved in the myocardial adaptation to overload and to unload.
80                          This induces Ca(2+) overload and ultimately the opening of the mitochondrial
81 survival have been shown to improve IE, iron overload, and anemia in animal models of BT.
82 elected as the outer shell to eliminate iron overload, and BMSCs implantation with high-molecular-wei
83 ained re-entrant excitation promoted calcium overload, and led to the emergence of focal excitations
84 ed lipid peroxidation, mitochondrial calcium overload, and mitochondrial dysfunction are characterist
85 ase by lowering pulmonary inflammation, iron overload, and mortality.
86 rized by accelerated atherosclerosis, volume overload, and progressive left ventricular hypertrophy,
87 estion, inflammatory cell infiltration, iron overload, and secretion of IL-6 in lavage fluid.
88 ar degree of hepcidin deficiency, serum iron overload, and tissue iron overload compared with single
89 tures of intra-articular inflammation, joint overloading, and tissue damage.
90 ial galactitol and galactonate after lactose overload appear to be good proxies for genetically deter
91 ve atrial remodeling during cardiac pressure overload are poorly defined.
92                    Animal models of pressure overload are valuable for understanding hypertensive hea
93 t risk of transfusion-associated circulatory overload as they are more frequently transfused and asso
94 nderlying causes of lung injury and/or fluid overload as well as from each other.
95 outside the cell, to avoid metal shortage or overload, as well as waste of metallophores.
96                                        Fluid overload at the initiation of continuous renal replaceme
97 , and they allow leakage of bile from the BS-overloaded biliary tract into blood, thereby protecting
98                Complications, including iron overload, bilirubin gallstones, extramedullary hematopoi
99             However, with long-term pressure overload both Atf6 and Atf6b null mice showed enhanced d
100 ined by the level of exposure to hemodynamic overload (both preload and afterload) as well as its int
101 Amyloid beta (Abeta) causes cytosolic Ca(2+) overload, but the effects of Abeta on mitochondrial Ca(2
102 jected to standardized pathological pressure overload by transverse aortic constriction (TAC) prior t
103 vanced age, or with documentation of volume "overload" by bedside examination.
104                                However, iron overload can damage the organism through a variety of me
105 the pathogenesis of several chronic pressure overload cardiac diseases.
106                                       Volume overload caused heart failure with decreased pyruvate de
107             Mechanical stretch due to muscle overload causes a restoration of fatigue resistance via
108                 In heart failure, myocardial overload causes vast metabolic changes that impair cardi
109 me overproduction of gratuitous proteins can overload cellular protein production resources, leading
110 ydrogel was fabricated for simultaneous iron overload clearance and bone marrow mesenchymal stem cell
111 y coefficient, distribution coefficient, and overload coefficient can significantly improve the destr
112 structed for the first time according to the overload coefficient, capacity parameter, weight coeffic
113 prolonged state of left ventricular pressure overload, commonly caused by hypertension and aortic val
114 ciency, serum iron overload, and tissue iron overload compared with single KO mice.
115 nregulated in the LA during cardiac pressure overload, contributing to both electrical and structural
116 sed a mouse model of left ventricle pressure overload coupled to in vitro studies in primary mouse an
117 enal syndrome type II, and with acute volume overload decompensation of the maternal circulation in l
118 igible that investigated the impact of fluid overload (defined by weight gain > 5%) or positive cumul
119  pathophysiologic conditions, such as volume overload, diabetes mellitus, and obesity, the cell biolo
120 ion with yacon flour, and phytate, in the Fe overloaded diets may exert a protective effect on these
121  function results in a rare form of the iron-overload disease hereditary hemochromatosis.
122           Interestingly, iron deficiency and overload disorders do not result in increased intestinal
123          Modeling results indicate initial N overload due to the lower C/N ratio in glyphosate compar
124          Importantly, this system can become overloaded due to ongoing environmental demands on the i
125 fective and safe in inducing control of iron overload during 12 months of treatment.
126 ress-responsive mechanism to limit (m)Ca(2+) overload during cardiac injury.
127 bioenergetic crisis and mitochondrial Ca(2+) overload during periods of nutrient stress.
128 inear weighted model of cascade failure with overloaded edges over synthetic and real weighted networ
129 ure in weighted complex networks considering overloaded edges to describe the redundant capacity for
130 e changes in our dietary pattern, dietary Pi overload engenders systemic phosphotoxicity, including e
131            At the behavioral level, training overload enhanced impulsivity in economic choice, which
132 mic patients affected by BT suffer from iron overload, even in the absence of chronic blood transfusi
133                            Results: Pressure overload evoked rapid left ventricular dilation compared
134 O mitochondria displayed a more rapid Ca(2+) overload, featuring an early opening of the mitochondria
135 rough altered intracellular Ca(2+) handling, overloading fetal cardiomyocyte intracellular Ca(2+) and
136 cognition and autonomous choice; information overload, finely tuned personalization and distorted soc
137 Accelerated systolic dysfunction in pressure-overloaded FS3KO mice was associated with accentuated ma
138 uated early systolic dysfunction in pressure-overloaded FS3KO mice, suggesting that the protective ef
139                                          The overload generated by the SS of the larger muscles group
140  adverse kidney events than those with fluid overload greater than 10% (71.6% vs 79.4%; p = 0.047).
141                                        Fluid overload greater than 10% was also found to be independe
142 riable logistic regression showed that fluid overload greater than 10% was associated with a 58% incr
143 portion of patients (95% CI) with peak fluid overload % greater than 10% and greater than 20% was 32.
144 nd its role in the mediation of hepatic iron overload has been dissected out.
145 in the standard murine nonischemic, pressure-overload heart failure model.
146 e can isolate diffuse leukocytes in pressure-overload heart failure.
147 cking PPP1R3A are protected against pressure-overload heart failure.
148 uates collagen cross-linking in the pressure-overloaded heart, leading to increased mortality, dilata
149 egular breathing patterns observed in volume overload HF and highlight their contribution to cardiac
150 l role in breathing irregularities in volume overload HF, and mediate the sympathetic responses induc
151 wley rats underwent surgery to induce volume overload HF.
152 jor factor driving progression from pressure-overload hypertrophy (POH) to HFpEF is the activation an
153  handling and PDE4B is decreased in pressure overload hypertrophy, suggesting that increasing PDE4B i
154                   Upon induction of pressure overload, immune activation occurs across the entire ran
155                       Concomitant mechanical overload improved both perfused capillary density and fa
156                           Hemolysis and iron overload improved upon iron chelation with full correcti
157 specific inhibitor successfully treated iron overload in a mouse model.
158                               Transient iron overload in adult mice infected with E. coli resulted in
159 tcomes of transfusion-associated circulatory overload in at least 10 ICU patients.
160                         SS increased cardiac overload in both performed orders.
161 tration goals and may help to prevent volume overload in critically ill patients.
162 l illness often results in significant fluid overload in critically ill patients.
163 aling axis in the LA during cardiac pressure overload in humans and mouse models and explore the role
164  (Dfx), which are already used to treat iron overload in humans, offer a new approach for treating AN
165 iology of transfusion-associated circulatory overload in ICU is not well characterized, leading to a
166 2 deficiency leads to cholesterol ester (CE) overload in microglia.
167 esults suggest that taming cytosolic calcium overload in pancreatic islets can improve beta-cell surv
168                                        Fluid overload in patients undergoing hemodialysis contributes
169 tcomes of transfusion-associated circulatory overload in PICU and adult ICU.
170 ammation, lung tissue inflammation, and iron overload in SCD.
171                          Mitochondrial lipid overload in skeletal muscle contributes to insulin resis
172 slation, thus reducing the misfolded protein overload in the ER.
173 ctors for transfusion-associated circulatory overload included positive fluid balance, the number and
174 ures, we found that reoxygenation or calcium overload increased brain ROS levels in a NOX5-dependent
175                                        Fluid overload % increased from median (interquartile range) 1
176              In contrast, body weight (fluid overload) increased already 5 days prior to continuous r
177                          We show that Ca(2+) overload induced by adrenergic stimulation of NCLX-null
178 shunt-induced PAH, and rats with RV pressure overload induced by pulmonary artery banding were treate
179 amine infusion and a 2-week chronic pressure overload induced by transverse aortic constriction (TAC)
180 s were significantly more tolerant to Ca(2+) overloading induced by high-frequency electrical pacing.
181 TAC) is a well-established model of pressure overload-induced cardiac hypertrophy and failure in mice
182 nt stages during the progression of pressure overload-induced cardiac hypertrophy in a mouse model, w
183 ne-stimulated cardiomyocytes and in pressure overload-induced cardiac hypertrophy in vivo.
184 tic constriction (TAC), a model for pressure overload-induced cardiac hypertrophy, and followed it by
185 overexpression of Gfat1 exacerbates pressure overload-induced cardiac hypertrophy, fibrosis, and card
186                                     Pressure overload-induced cardiac hypertrophy, such as that cause
187  vitro, endothelin-1- and, in vivo, pressure overload-induced cardiomyocyte hypertrophic growth is pr
188 ially imaged in the early stages of pressure-overload-induced heart failure and to compare the time c
189                                     Pressure overload-induced heart failure was established by transv
190 cific deletion of Lin28a attenuated pressure overload-induced hypertrophic growth, cardiac dysfunctio
191 iac fibrosis and dysfunction during pressure overload-induced hypertrophy and suggests that SAC/VAL s
192 e characterised a surgical model of pressure overload-induced hypertrophy in C57BL/6J mice produced b
193 ein abundance increased following functional overload-induced hypertrophy of the plantaris muscle in
194                              Often, pressure overload-induced myocardial remodeling does not undergo
195                                     Pressure overload-induced pathological cardiac hypertrophy is a c
196 iator of cardiac protection against pressure overload-induced pathological cardiac hypertrophy.
197 P4 gene deletion in mice attenuated pressure overload-induced pathological cardiac remodeling and hea
198                                         Iron overload (IO) is a common complication in BT patients af
199                                         Iron overload is a relatively common clinical condition resul
200                           The impact of this overload is deleterious to brain health, and it results
201           Transfusion-associated circulatory overload is frequent in ICU patients and is associated w
202                          Management of fluid overload is one of the most challenging problems in the
203           Transfusion-associated circulatory overload is the most frequent serious adverse transfusio
204 etardation, aminoaciduria, cholestasis, iron overload, lactic acidosis and early death (GRACILE syndr
205 ied to initiate re-entry and promote calcium overload, leading to the emergence of SCRE.
206                           Sustained pressure overload leads to dilative remodeling and systolic dysfu
207                                         iron overload leads to increased levels of toxic non-transfer
208                    Mechanistically, mtCa(2+) overload leads to increased mitochondrial reactive oxyge
209 ript levels of 109 genes important in volume-overload left ventricular remodeling with levels in norm
210                          Patients with fluid overload less than or equal to 10% were less likely to e
211 r-free days (p = 0.044), compared with fluid overload less than or equal to 10%.
212 k2-CKO) under tunicamycin stress or pressure overload manifested a defective ER response, cardiac dys
213                                  Moderate Fe overload may cause change in some liver markers (hemosid
214 nition of transfusion-associated circulatory overload may lead to a risk of underdiagnosis of this co
215 tions of the nanochelator for 5 days to iron overload mice and rats decrease iron levels in serum and
216 yo iron endowment in iron-sufficient or iron-overloaded mice, we generated combinations of mothers an
217                                              Overloading microglial lysosomes through myelin debris a
218       Downregulation of NCLX causes mtCa(2+) overload, mitochondrial depolarization, decreased expres
219 f chromatin organization with mouse pressure-overload model of myocardial stress (transverse aortic c
220 ified valves and in an experimental pressure overload model was assessed.
221 he RNA and protein levels in murine pressure overload models.
222 eostasis and generated mitochondrial calcium overload modifying mitochondrial function.
223 vated cardiac myofibroblasts in the pressure-overloaded myocardium are, at least in part, because of
224                              In the pressure-overloaded myocardium, TGF-beta/Smad3-activated cardiac
225  (n = 4), transfusion-associated circulatory overload (n = 7), transfusion-related acute lung injury
226                    In the era of information overload, natural language processing (NLP) techniques a
227                In mice subjected to pressure overload, nicotinamide riboside reduced cardiomyocyte de
228 etion is not the primary cause for manganese overload observed in individuals lacking functional ZIP1
229                                         Iron overload occurs in many hemorrhagic injuries due to hemo
230                                        Fluid overload (odds ratio, 1.08; 95% CI, 1.01-1.17) and need
231  0.42; CI, 0.29-0.60), or documented volume "overload" (odds ratio, 0.30; CI, 0.20-0.45) were less li
232  hematopoietic differentiation results in an overload of genotoxic stress, which causes aborted diffe
233 and over a longer timeframe, driving calcium overload of mitochondria to induce inflammation and dend
234 enario may be dependent on the intracellular overload of oxidized proteins.
235 ntersection between CAA and AD, representing overload of perivascular clearance pathways and the effe
236 ve higher mortality after sustained pressure overload of the heart, owing to mTORC1 hyperactivity tha
237 d tendon growth in adult mice via mechanical overload of the plantaris tendon.
238                                 We show that overloading of mitochondrial membrane carrier, but not m
239 ng immune tolerance, presumably activated by overloading of the organism with altered self-antigens.
240                                        Thus, overloading of the protein import machinery, rather than
241    And while the effect of excessive calcium overload on mitochondrial function is well appreciated,
242 t models for studying the impact of pressure overload on RV structure.
243 ron hypothesis' by showing that dietary iron overload or elevated non-transferrin bound iron (NTBI) a
244                          Prevention of Na(i) overload or inhibition of Na/Ca(mito) may be a new appro
245  myocardial fibrosis in response to pressure overload or myocardial infarction.
246 oride-sensing pathway (and not due to corpse overload or poor degradation), including the chloride-se
247 beyond that observed in response to pressure overload or Sirt3 deficiency alone.
248 llagen networks do fracture when tissues are overloaded or subject to pathological conditions such as
249 : endoplasmic reticulum (ER) stress, calcium overload, oxidative stress, and Abeta 1-42 oligomers tox
250 hermogenesis in NCLX-null BAT, while calcium overload persists.
251 ortance of YAP in response to acute pressure overload (PO).
252 in iron-deficient, iron-sufficient, and iron-overloaded pregnant women and children.
253                             Cardiac pressure overload produced a consistent downregulation of ErbB4,
254                       Protein misfolding and overloaded proteostasis networks underlie a range of neu
255 he reduction of energetic demands imposed by overload relief allowed the mitochondria to reduce its a
256 weeks, half of the banding animals underwent overload relief by an aortic debanding surgery (n=10).
257                                        Fluid overload represents a potentially modifiable risk factor
258 ophy are associated with pressure and volume overload, respectively, in cardiovascular disease both c
259 ut cannot overcome the ensuing hepatic lipid overload, resulting in fatty liver.
260 ROS landscape, we observed hemoglobin / iron overload, ROS production and lipid peroxidation in ectop
261 event ventricular dilatation in the pressure-overloaded RV.
262 is has a dual role in patients with pressure-overloaded RVs of idiopathic pulmonary arterial hyperten
263 tochondria from aging hearts develop calcium overload secondary to SR calcium leak.
264 g to red blood cell (RBC) transfusions, iron overload, shortened survival, and poor quality of life.
265 ment of procedures, new medications, sensory overload, sleep deprivation, prolonged bed rest, malnour
266 the heart was able to normalize the pressure overload-stimulated hypertrophic signals by activating G
267 of muscle performance following a mechanical overload stimulus indicates that angiogenic treatments t
268  right ventricle (RV) is subject to pressure overload stress, leading to RV hypertrophy and eventuall
269 portin activity can lead to diseases of iron overload, such as haemochromatosis, or iron limitation a
270 F-2alpha plays an important role during iron overload, systemic iron deficiency, and anemia.
271 ) are apparent using a trans-aortic pressure overload (TAC) model.
272 eas Smad158;Alb-Cre(+) mice had greater iron overload than Smad15;Alb-Cre(+) mice.
273 ar regulation mediated by VCP under pressure overload that may bring new insight into the mechanisms
274     Transfused patients frequently show iron overload that negatively affects hematopoiesis.
275                                    The toxin overloads the RPA pathway with ssDNA substrate, causing
276                To prevent detrimental Ca(2+) overload, the activity of MCU must be tightly regulated
277 esults suggest that in conditions of calcium overload, the vulnerable window of stretch-release to tr
278 ient mice in the presence or absence of iron overload to distinguish between the effects caused by a
279  homologous recombination (HR); however, DSB overload, together with massive end protection by 53BP1,
280 eactions, transfusion-associated circulatory overload, transfusion-related acute lung injury, and acu
281 a risk of transfusion-associated circulatory overload, transfusion-related acute lung injury, infecti
282  between 2 murine models of cardiac pressure overload, transverse aortic constriction banding and ang
283 ors, and the resultant mitochondrial calcium overload triggers cyclophilin-D-mediated necrosis.
284                                     Pressure overload triggers early activation of a matrix-synthetic
285 h-output heart failure was induced by volume overload using the arterio-venous fistula model (AV-Shun
286 nition of transfusion-associated circulatory overload varied among studies.
287  and dysfunction induced by chronic pressure overload via transverse aorta constriction or chronic ne
288   However, the role of CaMKIIdelta in volume overload (VO) has not been explored.
289 time point, adjusted relative risk for fluid overload was 2.79 (95% CI, 1.55-5.00) and 1.39 (95% CI,
290 f ICU stay, adjusted relative risk for fluid overload was 8.83 (95% CI, 4.03-19.33), and for cumulati
291                                        Fluid overload was assessed as fluid balance from admission to
292  replacement therapy, greater than 10% fluid overload was associated with higher risk of 90-day major
293                                        Fluid overload was associated with mortality in patients with
294 sfused patients, hepatic and myocardial iron overload was measured by multi-breath-hold MRI T2* and c
295                                   Peak fluid overload % was associated with greater PICU mortality (o
296                           Greater peak fluid overload % was associated with Major Adverse Kidney Even
297                               After pressure overload, we monitored the cardiac myocyte translatome b
298  through blood transfusions, leading to iron overload, which is a quite harmful consequence.
299 ntric cardiac remodeling induced by pressure overload, while inhibition of PP2A signaling prevents ec
300 rectomy; we also used AhR(-/-) knockout mice overloaded with indoxyl sulfate in drinking water.

 
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