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ABSTRACT: i-gel (Intersurgical Ltd., Wokingham, UK) is a new supraglottic airway device with a cuff made of thermoplastic elastomer gel. We retrospectively studied easiness of insertion and troubles in ventilation when this device was used by less experienced anesthesiologists. Consecutive eleven cases undergoing surgery under general anesthesia were studied. i-gel was successfully inserted in 7 cases (63%) at the first attempt, 2 cases at the second attempt without changing the size. In one case, the size was changed at the second attempt, which resulted in the successful insertion. There was one case of failed insertion even at the second attempt. Fiberoptic observation of the glottis showed direct contact of the cuff to the arytenoids cartilage in cases with successful insertion, however, spastic glottis, defined as contact of vocal cords was observed in 4 cases, and down-folding of the epiglottis was observed in 2 cases. During maintenance of anesthesia, ventilation trouble was observed in 3 cases. We conclude that i-gel should only be used with sufficient knowledge, preparations, skills or support from experienced physician to solve problems related to the safe use of supraglottic airway devices.
The Open Anesthesiology Journal 03/2013; 3(2):64-66.
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ABSTRACT: A train-of-four ratio (TOF ratio) of >0.9 should be the clinical cut-off to avoid residual paralysis. However, it is not rare to extubate patients without measurement of the TOF ratio, although the safe interval from the last administration of rocuronium assuring a TOF ratio of >0.9 has not been established in the daily clinical setting. In this study, to estimate the safe interval to avoid residual paralysis, we retrospectively selected patients in whom the TOF ratio was measured during remifentanil administration before extubation, and we studied the characteristics of recovery from the neuromuscular blockade produced by the empirical use of rocuronium.
Patients undergoing surgery under general anesthesia with sevoflurane and remifentanil were studied (n = 134). Rocuronium was administered at 0.7-1.0 mg/kg for tracheal intubation, and repeated bolus administration (10 mg) or continuous infusion (15-25 mg/h) was performed by the anesthesiologists in charge of the patient to maintain intraoperative paralysis. At the end of the surgery, the TOF ratio was measured, during remifentanil infusion and the contribution of clinical parameters to spontaneous recovery from the rocuronium-induced paralysis was studied by multivariate logistic regression analyses.
Spontaneous recovery from rocuronium-induced paralysis within 2 h after the last administration of rocuronium varied among the patients. Multivariate logistic regression analyses showed that age (P = 0.002) and time elapsed from the last administration of rocuronium (P < 0.0001) significantly contributed to TOF recovery, and elderly patients demonstrated significantly slower recovery.
Because of the large variation in the recovery from rocuronium-induced paralysis, TOF-based evaluation of residual paralysis is essential to determine the appropriate indication for reversal, especially for elderly patients.
Journal of Anesthesia 09/2011; 25(6):845-9. · 0.83 Impact Factor
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ABSTRACT: Neurological deficits associated with methylergometrine have been reported primarily as a result of reversible cerebral vasoconstriction syndromes (RCVS). RCVS are characterized by reversible multifocal vasoconstrictions of the cerebral arteries heralded by acute severe headache with or without neurological deficits. Here, we present the first case of suspected RCVS with transient limb myoclonus following the intravenous administration of methylergometrine during cesarean section. A 31-year-old woman who received slowly infused intravenous methylergometrine during a cesarean section suddenly reported severe occipital headache after 40 min, followed by apnea and unconsciousness for 8 min. A second administration of methylergometrine to treat the weakness of her uterine contractions resulted in a repeated loss of consciousness within minutes and the development of limb myoclonus. No abnormalities were detected by brain computerized tomography, magnetic resonance imaging, and electroencephalogram. She fully recovered spontaneously within 12 h. We consider that the transient limb myoclonus in our patient appeared as a result of RCVS caused by the intravenous administration of methylergometrine.
Journal of Anesthesia 03/2011; 25(3):405-8. · 0.83 Impact Factor
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Tokujiro Uchida
Journal of Anesthesia 02/2011; 25(1):152-4. · 0.83 Impact Factor
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ABSTRACT: Although the receptor for advanced glycation end products (RAGE) has been used as a biological marker of alveolar epithelial cell injury in clinical studies, the mechanism for release of soluble RAGE from lung epithelial cells has not been well studied. Therefore, these studies were designed to determine the mechanism for release of soluble RAGE after lipopolysaccharide (LPS) challenge. For these purposes, alveolar epithelial cells from rat lungs were cultured on Transwell inserts, and LPS was added to the apical side (500 μg/ml) for 16 h on day 7. On day 7, RAGE was expressed predominantly in surfactant protein D-negative cells, and LPS challenge induced release of RAGE into the medium. This response was partially blocked by matrix metalloproteinase (MMP) inhibitors. Transcripts of MMP-3 and MMP-13 were upregulated by LPS, whereas RAGE transcripts did not change. Proteolysis by MMP-3 and MMP-13 resulted in soluble RAGE expression in the bronchoalveolar lavage fluid in the in situ rat lung, and this reaction was inhibited by MMP inhibitors. In human studies, both MMP-3 and -13 antigen levels were significantly correlated with the level of RAGE in pulmonary edema fluid samples. These results support the conclusion that release of RAGE is primarily mediated by proteolytic damage in alveolar epithelial cells in the lung, caused by proteases in acute inflammatory conditions in the distal air spaces.
AJP Lung Cellular and Molecular Physiology 01/2011; 300(4):L516-25. · 3.66 Impact Factor
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ABSTRACT: Cardiopulmonary resuscitation (CPR) in the lateral position during noncardiac surgery has been described in only a few reports in the past. Here, we report a case of cardiac arrest in a 61-year-old man undergoing microvascular decompression surgery for trigeminal neuralgia in the left lateral decubitus position. During the initial 5 min of CPR, chest compression was performed in this position by two rescuers; one from the chest and the other from the back, pushing simultaneously. Because ventricular arrhythmia was refractory to conventional CPR even after placing the patient back to the supine position, extracorporeal life support was introduced in the operating room by using the femoro-femoral approach (right atrio-femoral veno-arterial bypass). This alternative CPR markedly decreased the frequency of ventricular arrhythmia. Subsequent coronary angiogram detected 99% stenosis of the right coronary artery. Ventricular arrhythmia ceased after coronary revascularization, and the patient was successfully weaned from the extracorporeal bypass circuit. The patient was discharged alive with minimal neurological impairment. We suggest that chest compression in the lateral position by two rescuers is an efficient resuscitation maneuver, and if an electrical storm is refractory to conventional CPR, extracorporeal life support should be considered in the operating-room setting.
Journal of Anesthesia 03/2010; 24(3):447-51. · 0.83 Impact Factor
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ABSTRACT: A patient developed anaphylactic shock after a heparin dosage during an operation to make inner shunt for chronic renal failure of Alport syndrome. The operation was canceled and the patient was admitted to the ICU with tracheal intubation. He was extubated safely on the fifth postoperative day, but he lost the sense of smell from the day after. Abnormality of the nasal mucosa was not recognized. The smell disorder improved slowly in three or four weeks. Anosmia after anaphylactic shock is very rare, but we should be careful for this complication after anaphylactic shock.
Masui. The Japanese journal of anesthesiology 09/2009; 58(8):997-9.
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ABSTRACT: Although alveolar epithelial injury is a major determinant of outcome in patients with acute lung injury, there is no reliable biological marker of alveolar epithelial injury. The primary objective was to determine whether elevated levels of the receptor for advanced glycation end products (RAGE), a marker of alveolar epithelial injury, reflect impaired alveolar fluid clearance (AFC) in an ex vivo perfused human lung preparation. A second objective was to determine whether levels of a marker of endothelial injury, von Willebrand factor antigen (vWF:Ag), are associated with impaired AFC.
Human lungs (N = 30) declined for transplantation by the California Transplant Donor Network were perfused at a constant pulmonary artery pressure of 12 mm Hg. Following rewarming to 36 degrees C, the lungs were inflated with a continuous positive airway pressure of 10 cm H(2)O. RAGE and vWF:Ag levels and AFC rates were then measured.
The rate of AFC was inversely correlated with RAGE levels in the alveolar fluid (p < 0.005). Similarly, the concentration of RAGE in the alveolar fluid was significantly higher in lungs with submaximal AFC, defined in a prespecified analysis as <or= 14%/h, when compared with lungs with preserved AFC (median 0.82 vs 0.43 microg/mL; p < 0.05). In contrast, vWF:Ag levels did not correlate with the rate of AFC.
RAGE may be a useful biological marker of alveolar epithelial injury and impaired AFC in donor lungs prior to transplant and perhaps in patients with acute lung injury.
Chest 11/2008; 135(2):269-75. · 5.25 Impact Factor
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ABSTRACT: Since its original definition forty years ago, acute lung injury/acute respiratory distress syndrome has been a challenging target for both clinicians and researchers. In this review, several progresses in the past decades in the area of research concerning the pathophysiology of alveolar epithelium in this syndrome are discussed. Understanding the mechanism of tissue injury and tissue repair are key points to develop new strategy for clinical evaluation of severity of this syndrome and possible therapeutic approaches in future.
Masui. The Japanese journal of anesthesiology 02/2008; 57(1):51-9.
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ABSTRACT: New evidence indicates that neural mechanisms can down-regulate acute inflammation. In these studies, we tested the potential role of the alpha7 nicotinic acetylcholine receptor (alpha7 nAChR) in a rodent model of acid-induced acute lung injury. We first determined that the alpha7 nAChR was expressed by alveolar macrophages and lung epithelial cells. Then, using an acid-induced acute lung injury mouse model, we found that nicotine, choline, and PNU-282,987 (a specific alpha7 nAChR agonist) decreased excess lung water and lung vascular permeability, and reduced protein concentration in the bronchoalveolar lavage (BAL). Deficiency of alpha7 nAChR resulted in a 2-fold increase in excess lung water and lung vascular permeability. The reduction of proinflammatory cytokines (macrophage inflammatory protein-2 and TNF-alpha) in the BAL with nicotine probably resulted from the suppression of NF-kappaB activation in alveolar macrophages. The beneficial effect of nicotine was also tested in rat model of acid-induced acute lung injury in which BAL protein and receptor for advanced glycation end products (RAGE), a marker of type I cell injury, were reduced by nicotine treatment. These results indicate that activation of alpha7 nAChR may provide a new therapeutic pathway for the treatment of acute lung injury.
American Journal of Respiratory Cell and Molecular Biology 09/2007; 37(2):186-92. · 5.13 Impact Factor
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Carolyn S Calfee,
Marie M Budev,
Michael A Matthay,
Gwynne Church,
Sandra Brady, Tokujiro Uchida,
Akitoshi Ishizaka,
Abigail Lara,
Justin L Ranes,
Malcom M deCamp,
Alejandro C Arroliga
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ABSTRACT: Primary graft dysfunction, formerly termed reperfusion pulmonary edema, is the leading cause of short-term complications after lung transplantation. New evidence shows that alveolar type I epithelial cells play an active role in alveolar fluid transport and are therefore presumed to be critical in the absorption of pulmonary edema. We tested the potential relevance of a novel marker of alveolar type I cell injury, the receptor for advanced glycation end-products (RAGE), to short-term outcomes of lung transplantation.
The study was a prospective, observational cohort study of 20 patients undergoing single lung, bilateral lung or combined heart-lung transplantation. Plasma biomarkers were measured 4 hours after allograft reperfusion.
Higher plasma RAGE levels were associated with a longer duration of mechanical ventilation and longer intensive care unit length of stay, in contrast to markers of alveolar type II cell injury, endothelial injury and acute inflammation. Specifically, for every doubling in plasma RAGE levels, the duration of mechanical ventilation increased on average by 26 hours, adjusting for ischemia time (95% confidence interval [CI] 7.4 to 44.7 hours, p = 0.01). Likewise, for every doubling of plasma RAGE levels, intensive care unit length of stay increased on average by 1.8 days, again adjusting for ischemia time (95% CI 0.13 to 3.45 days p = 0.04). In contrast, the clinical diagnosis of primary graft dysfunction was not as predictive of these short-term outcomes.
Higher levels of plasma RAGE measured shortly after reperfusion predicted poor short-term outcomes from lung transplantation. Elevated plasma RAGE levels may have both pathogenetic and prognostic value in patients after lung transplantation.
The Journal of heart and lung transplantation: the official publication of the International Society for Heart Transplantation 08/2007; 26(7):675-80. · 3.54 Impact Factor
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ABSTRACT: To study air space fluid clearance (AFC) under conditions that resemble the clinical setting of pulmonary edema in patients, we developed a new perfused human lung preparation. We measured AFC in 20 human lungs rejected for transplantation and determined the contribution of AFC to lung fluid balance. AFC was then compared with air space and perfusate levels of a biological marker of epithelial injury. The majority of human lungs rejected for transplant had intact basal (75%) and beta(2)-adrenergic agonist-stimulated (70%) AFC. For lungs with both basal and stimulated AFC, the basal AFC rate was 19 +/- 10%/h, and the beta(2)-adrenergic-stimulated AFC rate was 43 +/- 13%/h. Higher rates of AFC were associated with less lung weight gain (Pearson coefficient -0.90, P < 0.0001). Air space and perfusate levels of the type I pneumocyte marker receptor for advanced glycation end products (RAGE) were threefold and sixfold higher, respectively, in lungs without basal AFC compared with lungs with AFC (P < 0.05). These data show that preserved AFC is a critical determinant of favorable lung fluid balance in the perfused human lung, raising the possibility that beta(2)-agonist therapy to increase edema fluid clearance may be of value for patients with acute lung injury and pulmonary edema. Also, although additional studies are needed, a biological marker of alveolar epithelial injury may be useful clinically in predicting preserved AFC.
AJP Lung Cellular and Molecular Physiology 07/2007; 293(1):L52-9. · 3.66 Impact Factor
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ABSTRACT: Receptor for advanced glycation end-products (RAGE) is one of the alveolar type I cell-associated proteins in the lung.
To test the hypothesis that RAGE is a marker of alveolar epithelial type I cell injury.
Rats were instilled intratracheally with 10 mg/kg lipopolysaccharide or hydrochloric acid. RAGE levels were measured in the bronchoalveolar lavage (BAL) and serum in the rats and in the pulmonary edema fluid and plasma from patients with acute lung injury (ALI; n = 22) and hydrostatic pulmonary edema (n = 11).
In the rat lung injury studies, RAGE was released into the BAL and serum as a single soluble isoform sized approximately 48 kD. The elevated levels of RAGE in the BAL correlated well with the severity of experimentally induced lung injury. In the human studies, the RAGE level in the pulmonary edema fluid was significantly higher than the plasma level (p < 0.0001). The median edema fluid/plasma ratio of RAGE levels was 105 (interquartile range, 55-243). The RAGE levels in the pulmonary edema fluid from patients with ALI were higher than the levels from patients with hydrostatic pulmonary edema (p < 0.05), and the plasma RAGE level in patients with ALI were significantly higher than the healthy volunteers (p < 0.001) or patients with hydrostatic pulmonary edema (p < 0.05).
RAGE is a marker of type I alveolar epithelial cell injury based on experimental studies in rats and in patients with ALI.
American Journal of Respiratory and Critical Care Medicine 05/2006; 173(9):1008-15. · 11.08 Impact Factor
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ABSTRACT: A 77-year-old man was scheduled to undergo a cervical lymph node biopsy under general anesthesia. Although awake, nasotracheal fiberoptic intubation was initially planned because of an anticipated difficult airway, the attempt was unsuccessful. Orotracheal intubation was subsequently performed under direct laryngoscopy without difficulty. After initiating positive pressure mechanical ventilation, subcutaneous and mediastinal emphysema developed. The cause of this emphysema was considered to be tracheal perforation after an unsuccessful attempt at fiberoptic tracheal intubation.
Journal of Clinical Anesthesia 04/2006; 18(2):135-7. · 1.21 Impact Factor
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ABSTRACT: The amiloride-sensitive epithelial sodium channel (ENaC) constitutes a rate-limiting step for sodium (Na+) and water absorption across lung alveolar epithelium. Recent reports suggested that ENaC is regulated by membrane-bound extracellular serine proteases, such as channel-activating proteases (CAPs). The objectives of this study were to examine the role of serine proteases in the regulation of transepithelial alveolar Na+ and water transport in vitro and in vivo and the expression of CAPs in rodent distal lung. In vitro experiments showed that inhibition of endogenous serine proteases by apical aprotinin 1) decreased ENaC-mediated currents in primary cultures of rat and mouse alveolar epithelial cells without affecting the abundance nor the electrophoretic migration pattern of biotinylated alpha- and beta-ENaC expressed at the cell surface and 2) suppressed the increase in amiloride-sensitive short-circuit current induced by the beta2-agonist terbutaline. RT-PCR experiments indicated that CAP1, CAP2, and CAP3 mRNAs were expressed in mouse alveolar epithelial cells, whereas CAP1 was also expressed in alveolar macrophages recovered by bronchoalveolar lavage. CAP1 protein was detected by Western blotting in rat and mouse alveolar epithelial cells, alveolar macrophages and bronchoalveolar lavage fluid. Finally, in vivo experiments revealed that intra-alveolar treatment with aprotinin abolished the increase in Na+-driven alveolar fluid clearance (AFC) induced by terbutaline in an in situ mouse lung model, whereas trypsin potentiated it. These results show that endogenous membrane-bound and/or secreted serine proteases such as CAPs regulate alveolar Na+ and fluid transport in vitro and in vivo in rodent lung.
AJP Lung Cellular and Molecular Physiology 07/2005; 288(6):L1099-109. · 3.66 Impact Factor
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Canadian Journal of Anaesthesia 06/2005; 52(6):660-661. · 2.35 Impact Factor
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ABSTRACT: Cerebellar hemorrhage is an unpredictable complication of spinal surgery. We encountered a case of cerebellar hemorrhage presenting with delayed emergence from anesthesia and hemiplegia after resection of an intradural extramedullar tumor from the cervical spine. Postoperative brain computed tomography revealed hematoma in the cerebellar vermis and right cerebellar hemisphere. The patient made a gradual recovery with conservative treatment. Although the mechanism of cerebellar hemorrhage remains speculative, loss of cerebrospinal fluid may play an important role. Cerebellar hemorrhage must therefore be considered in patients with unexplained neurological deterioration or disturbance on emergence from anesthesia after spinal surgery.
Anesthesia & Analgesia 06/2005; 100(5):1470-1, table of contents. · 3.29 Impact Factor
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ABSTRACT: A 13-month-old girl with cyanotic congenital heart disease; single atrium, single ventricle, common atrioventricular (AV) valve, pulmonary atresia and total anomalous pulmonary venous drainage, suspected of asplenia underwent ear tube surgery for otitis media. She had undergone bilateral Blalock-Taussig shunts for her heart disease. She had congestive heart failure due to moderate to severe common AV valve regurgitation and often experienced respiratory tract infection with sputum. Oxyhemoglobin saturation measured by pulse oximetry was 75-80% and polycythemia was found in complete blood count. We chose tracheal intubation for her airway management because of a large amount of sputum. General anesthesia was maintained with sevoflurane, nitrous oxide and oxygen for ear tube surgery. During anesthesia she showed several episodes of desaturation which were well managed by frequent tracheal suctioning. Her circulation was stable with 50% N2O and sevoflurane 1.7-2.0%. The operation was performed uneventfully and the patient was discharged to the ward after tracheal extubation. Asplenia is frequently complicated with cyanotic congenital heart disease and increased susceptibility to bacterial infection. Anesthesia for these patients with upper respiratory infection should be managed with tracheal intubation even for a short surgery.
Masui. The Japanese journal of anesthesiology 04/2005; 54(3):304-7.
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ABSTRACT: Transcriptional adaptations to hypoxia are mediated by hypoxia-inducible factor (HIF)-1, a heterodimer of HIF-alpha and aryl hydrocarbon receptor nuclear translocator subunits. The HIF-1alpha and HIF-2alpha subunits both undergo rapid hypoxia-induced protein stabilization and bind identical target DNA sequences. When coexpressed in similar cell types, discriminating control mechanisms may exist for their regulation, explaining why HIF-1alpha and HIF-2alpha do not substitute during embryogenesis. We report that, in a human lung epithelial cell line (A549), HIF-1alpha and HIF-2alpha proteins were similarly induced by acute hypoxia (4 h, 0.5% O(2)) at the translational or posttranslational level. However, HIF-1alpha and HIF-2alpha were differentially regulated by prolonged hypoxia (12 h, 0.5% O(2)) since HIF-1alpha protein stimulation disappeared because of a reduction in its mRNA stability, whereas HIF-2alpha protein stimulation remained high and stable. Prolonged hypoxia also induced an increase in the quantity of natural antisense HIF-1alpha (aHIF), whose gene promoter contains several putative hypoxia response elements to which (as we confirm here) the HIF-1alpha or HIF-2alpha protein can bind. Finally, transient transfection of A549 cells by dominant-negative HIF-2alpha, also acting as a dominant-negative for HIF-1alpha, prevented both the decrease in the HIF-1alpha protein and the increase in the aHIF transcript. Taken together, these data indicate that, during prolonged hypoxia, HIF-alpha proteins negatively regulate HIF-1alpha expression through an increase in aHIF and destabilization of HIF-1alpha mRNA. This trans-regulation between HIF-1alpha and HIF-2alpha during hypoxia likely conveys target gene specificity.
Journal of Biological Chemistry 05/2004; 279(15):14871-8. · 4.77 Impact Factor
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ABSTRACT: Transcriptional adaptations to hypoxia are mediated by hypoxia-inducible factor (HIF)-1, a heterodimer of HIF-α and aryl hydrocarbon
receptor nuclear translocator subunits. The HIF-1α and HIF-2α subunits both undergo rapid hypoxia-induced protein stabilization
and bind identical target DNA sequences. When coexpressed in similar cell types, discriminating control mechanisms may exist
for their regulation, explaining why HIF-1α and HIF-2α do not substitute during embryogenesis. We report that, in a human
lung epithelial cell line (A549), HIF-1α and HIF-2α proteins were similarly induced by acute hypoxia (4 h, 0.5% O2) at the translational or posttranslational level. However, HIF-1α and HIF-2α were differentially regulated by prolonged hypoxia
(12 h, 0.5% O2) since HIF-1α protein stimulation disappeared because of a reduction in its mRNA stability, whereas HIF-2α protein stimulation
remained high and stable. Prolonged hypoxia also induced an increase in the quantity of natural antisense HIF-1α (aHIF), whose
gene promoter contains several putative hypoxia response elements to which (as we confirm here) the HIF-1α or HIF-2α protein
can bind. Finally, transient transfection of A549 cells by dominant-negative HIF-2α, also acting as a dominant-negative for
HIF-1α, prevented both the decrease in the HIF-1α protein and the increase in the aHIF transcript. Taken together, these data
indicate that, during prolonged hypoxia, HIF-α proteins negatively regulate HIF-1α expression through an increase in aHIF
and destabilization of HIF-1α mRNA. This trans-regulation between HIF-1α and HIF-2α during hypoxia likely conveys target gene specificity.
Journal of Biological Chemistry 04/2004; 279(15):14871-14878. · 4.77 Impact Factor
