Biomedical subjects

A Maki

Publications and source records attributed to A Maki.

At least 37 records · Page 2Linked to original sources

PubMed1998

Mucosal bile duct carcinoma with superficial spread.

We describe a case of mucosal bile duct carcinoma with superficial spread in a 69-year-old man with gallstone pancreatitis. The patient was seen at the hospital because of abdominal pain, fever, and jaundice. Endoscopic retrograde cholangiography (ERC) demonstrated a protruding lesion in the lower third of the common bile duct (CBD) showing wall irregularity suggestive of malignancy. Percutaneous transhepatic cholangioscopy (PTCS) disclosed a papillary tumor with granular mucosa extending continuously to the middle third of the CBD. Cholangioscopic biopsy specimens taken from both the papillary tumor and surrounding granular mucosa revealed papillary adenocarcinoma. After this assessment of extent of cancer by PTCS, we performed pancreatoduodenectomy with extrahepatic bile duct resection and regional lymph node dissection. Pathology examination revealed papillary adenocarcinoma limited to the mucosal layer. The resected margin of the bile duct was free of tumor. We also reviewed 25 cases of early mucosal bile duct carcinoma described in detail in the Japanese literature, and we discuss the diagnostic advantages of PTCS.

Adenocarcinoma, Papillary↗

PubMed1998

Human platelet activation by thrombolytic agents: effects of tissue-type plasminogen activator and urokinase on platelet surface P-selectin expression.

The mechanisms that underlie reocclusion during thrombolytic therapy have not yet been clarified. The purpose of this study was to investigate the activating effects of tissue-type plasminogen activator and urokinase and the inhibitory effects of acetylsalicylic acid by measuring platelet surface P-selectin as a marker of platelet activation. After addition of urokinase (final concentration 192 U/ml, 1920 U/ml, or 19,200 U/ml) or tissue-type plasminogen activator (final concentration 120 U/ml, 1200 U/ml, or 12,000 U/ml) to platelet-rich plasma from 12 healthy persons, platelet surface P-selectin expression was measured by means of flow cytometry with an anti-CD62 monoclonal antibody. The presence of urokinase and tissue-type plasminogen activator increased platelet surface P-selectin expression in a concentration-dependent manner. In the next step, either 160 mg/day (n = 6) or 660 mg/day (n = 6) acetylsalicylic acid was administered to the 12 healthy persons, and venous blood samples were collected after 7 days of treatment. Platelet surface P-selectin expression was measured with the method used earlier and after addition of tissue-type plasminogen activator or urokinase. Although the effect of acetylsalicylic acid at 160 mg/day on P-selectin expression was minimal, a dose of 660 mg/day suppressed platelet P-selectin expression and inhibited the platelet activating effects of tissue-type plasminogen activator and urokinase in a statistically significant way. Platelets were activated by tissue-type plasminogen activator or urokinase, and this platelet activation was suppressed with administration of acetylsalicylic acid at 660 mg/day.

Aspirin↗

PubMed1998

Cerebral blood volume in the sleep measured by near-infrared spectroscopy.

We investigated the relationship between hemodynamic changes in the cortex measured by near-infrared spectroscopy (NIRS) and the polysomnographic changes during sleep. Four healthy male volunteers participated in the study. Near-infrared spectroscopy measuring and polysomnographic recordings were done simultaneously during sleep. In many case, oxy-hemoglobin (oxy-Hb) decreased and deoxy-hemoglobin (deoxy-Hb) increased during the transition from wakefulness to sleep, and oxy-Hb increased toward deep sleep. Oxy-Hb and deoxy-Hb had larger fluctuations during REM sleep than those during non-REM sleep. During REM sleep, oxy-Hb often showed a lower level and deoxy-Hb showed a higher level than those during the preceding and following non-REM sleep.

Adult↗

PubMed1998

Mechanism of rethrombosis after thrombolytic therapy: angioscopic findings and investigation of the coagulation system in dogs.

The purpose of this study was to angioscopically observe the process of thrombolysis after intracoronary administration of thrombolytic agents and to investigate the effects of these agents on coagulation/fibrinolysis systems in dogs. The coronary endothelium was removed and thrombus formation was confirmed by angioscopy. In the tissue plasminogen activator (tPA) group (n=8), complete thrombolysis occurred in all animals, but thrombolysis was incomplete in the urokinase (UK) group (n=6). The plasma level of plasmin alpha2-plasmin inhibitor complex peaked at 15 minutes after treatment in both the tPA and UK groups. Plasma thrombin-antithrombin III (TAT) complex decreased transiently at 15 minutes after tPA administration but increased at 30 and 60 minutes (P<0.05). In the UK group, plasma TAT also showed a transient decrease followed by an increase, which was minimal compared with that in the tPA group. Plasma TAT decreased transiently after infusion of tPA and subsequently increased to above the pretreatment level, suggesting a risk of rethrombosis after successful recanalization.

Angioscopy↗

PubMed1997

Clinical and prognostic significance of atrial fibrillation in acute myocardial infarction.

The clinical significance of the time of onset of atrial fibrillation (AF) was investigated in patients with acute myocardial infarction (AMI). Among 1,039 patients with AMI, 100 (9.6%) had AF. These patients were divided into 3 groups: AF group 1 (n = 45), who developed AF within 24 hours of the onset of AMI; AF group 2 (n = 41), who developed AF >24 hours after the onset of AMI; and AF group 3 (n = 14), who developed AF before the onset of AMI. The infarct-related lesion was most frequent (67%) in the proximal right coronary artery in AF group 1 (p <0.01). Right atrial pressure was most significantly increased in AF group 1. The left atrial dimension and pulmonary arterial wedge pressure were most significantly increased, and left ventricular ejection fraction was most significantly decreased in AF group 2. In the acute phase, the frequencies of heart failure, cardiogenic shock, and in-hospital mortality were higher for all 3 AF groups than the sinus group (p <0.01). The long-term survival rate was significantly lower in AF group 1 and AF group 2 than in the sinus group. AF was an independent predictor of cardiac death in both AF group 1 (odds ratio 2.5; 95% confidence interval 1.2 to 5.0; p = 0.0012) and AF group 2 (odds ratio 3.7; 95% confidence interval 1.8 to 7.5; p = 0.0005), but not in AF group 3. The onset time of AF appears to be a useful parameter for evaluating the cardiac status and prognosis of patients with AMI.

Aged↗

PubMed1997

Prognostic significance of a clearly audible fourth heart sound detected a month after an acute myocardial infarction.

Patients (n = 181) with a myocardial infarction, with (n = 20) or without (n = 161) a clearly audible fourth heart sound detected 1 month after the onset of a myocardial infarction, were followed for 56.2 +/- 21.4 months for cardiac events (death, myocardial infarction, percutaneous transluminal coronary angioplasty, coronary artery bypass surgery, worsening angina, or heart failure). The present study suggests that a clearly audible fourth heart sound detected 1 month after the onset of myocardial infarction increases the risk of adverse cardiac events.

Aged↗

PubMed1997

Intensity Measurements of Deltal > 1 Transitions of Several Isotopomers of HCN

The intensities of the forbidden Q-branch transitions 02(2f)0-00(0)0, 12(2f)0-00(0)0, and 02(2f)1-00(0)0 for HCN have been measured. The intensities of the 02(2f)0-00(0)0 transitions of DCN, D13C15N, and H12C15N were also measured, as well as the 02(2f)1-00(0)0 transitions of H12C15N and H13C15N. These Q-branch transitions are forbidden even when the effects of l-type resonance are considered so they must get their intensity from some other Coriolis interactions. The much stronger P- and R-branch lines for the e levels of these same vibrational transitions were also measured and they are shown to get most of their intensity from l-type resonance. However, the same Coriolis resonance that gives intensity to the Q-branch transitions seems to affect the DeltaJ = ±1 transitions as shown by the difference in the intensities of the DeltaJ = +1 and DeltaJ = -1 transitions. Measurements of the intensity of the 03(3e)0-00(0)0 and 03(3f)0-00(0)0 transitions shows that they derive most, but perhaps not all, of their intensity from l-type resonance. An unsuccessful search for forbidden DeltaJ = 0, e-e transitions for the strong 10(0)0-00(0)0 band shows that there is no detectable mixing of the e and f levels. Copyright 1997 Academic Press. Copyright 1997Academic Press

Journal Article↗

PubMed1997

Platelet-dependent thrombin generation in patients with hyperlipidemia.

OBJECTIVES: We evaluated coagulability as determined by platelet-dependent thrombin generation in hypercholesterolemic patients before and after treatment with pravastatin and in hypertriglyceridemic patients to investigate the usefulness of coagulability as an index of atherosclerosis and to determine the importance of treating hyperlipidemia. BACKGROUND: An understanding of the interaction between platelets and the plasma coagulation system is important for clarifying the mechanism of the procoagulant process. METHODS: We assessed coagulability in 58 patients with hypercholesterolemia (serum total cholesterol level > or = 220 mg/dl, age 56.5 +/- 1.5 years [mean +/- SEM]), 37 patients with hypertriglyceridemia (serum triglyceride level > or = 200 mg/dl, age 59.5 +/- 1.7 years), 13 patients with hypercholesterolemia plus hypertriglyceridemia (age 51.4 +/- 3.1 years) and 75 normal subjects (age 52.2 +/- 1.7 years). We also studied platelet-dependent thrombin generation in patients with hypercholesterolemia before and after treatment with pravastatin. Calcium chloride was added to 0.5 ml of platelet-rich plasma (150 x 10(9)/liter) to initiate coagulation. Ten microliters of the sample was transferred into 90 microliters of 3.8% sodium citrate at 10-min intervals for 30 min. A chromogenic substrate, S-2238, was added to each sample, and absorbance was measured spectrophotometrically at a wavelength of 405 nm to determine thrombin generation. RESULTS: Platelet-dependent thrombin generation was increased in patients with hypercholesterolemia and patients with hypercholesterolemia plus hypertriglyceridemia (p < 0.01) compared with patients with hypertriglyceridemia and control subjects. Treatment with pravastatin normalized thrombin generation. CONCLUSIONS: Hypercholesterolemia, but not hypertriglyceridemia, was associated with increased platelet-dependent thrombin generation. Pravastatin normalized the generation of thrombin.

Adult↗

PubMed1997

Lack of delayed effects of amphetamine, methoxamine, and prazosin (adrenergic drugs) on behavioral outcome after lateral fluid percussion brain injury in the rat.

This study examined the delayed effects of the administration of d-amphetamine, methoxamine (an alpha1-adrenergic receptor agonist), and prazosin (an alpha1-adrenergic receptor antagonist) on the behavioral outcome of lateral fluid-percussion (FP) brain injury. Rats trained to perform a beam-walking task were subjected to brain injury of moderate severity (2.1 to 2.2 atm). Twenty-four hours after injury, rats were treated with amphetamine, methoxamine, or prazosin at two or three different dose levels. Amphetamine-treated animals displayed no significant improvement in beam-walking ability either during or after drug intoxication (from days 3 to 5 after brain injury). Similarly, neither methoxamine nor prazosin significantly affected beam-walking ability during or after drug intoxication. Neither amphetamine treatment at three different doses nor treatment with methoxamine or prazosin at two different doses affected the spatial learning disabilities of brain-injured animals. These results suggest that (1) unlike amphetamine administration after sensorimotor cortex (SMC) ablation or contusion brain injury models, amphetamine administration at 24 h after concussive FP brain injury does not improve beam-walking performance; (2) unlike amphetamine administration 10 min after concussive FP brain injury amphetamine administration 24 h after injury does not improve cognitive function; and (3) unlike prazosin administration after SMC ablation brain injury, prazosin administration 24 h after concussive FP brain injury does not effect beam-walking performance.

Amphetamine↗

PubMed1997

Effects of six weeks of chronic ethanol administration on lactic acid accumulation and high energy phosphate levels after experimental brain injury in rats.

The effects of 6 weeks of chronic ethanol administration on the lateral fluid percussion (FP) brain injury-induced regional accumulation of lactate and on the levels of total high-energy phosphates were examined in rats. In both the chronic ethanol diet (ethanol diet) and pair-fed isocaloric sucrose control diet (control diet) groups, tissue concentrations of lactate were elevated in the cortices and hippocampi of both the ipsilateral and contralateral hemispheres at 5 min after brain injury. In both diet groups, concentrations of lactate were elevated only in the injured left cortex and the ipsilateral hippocampus at 20 min after FP brain injury. No significant differences were found in the levels of lactate in the cortices and hippocampi of sham animals and brain-injured animals between the ethanol and control diet groups at 5 min and 20 min after injury. In the ethanol and control diet groups, tissue concentrations of total high-energy phosphates (ATP + PCr) were not affected in the cortices and hippocampi at 5 min and 20 min after lateral FP brain injury. No significant differences were found in the levels of total high-energy phosphates in the cortices and hippocampi of the sham and brain-injured animals between the ethanol and control diet groups at 5 min and 20 min after injury. Histologic studies revealed a similar extent of damage in the cortex and in the CA3 region of the ipsilateral hippocampus in both diet groups at 14 days after lateral FP brain injury. These findings suggest that 6 weeks of chronic ethanol administration does not alter brain injury-induced accumulation of lactate, levels of total high energy phosphates, and extent of morphological damage.

Adenosine Triphosphate↗

PubMed1997

Nonradioactive in situ hybridization histochemistry in leukemic and nonleukemic culture.

Technical limitations are associated with conducting successful in situ hybridization. In this study, three cell types including a tumor neuroblastoma cell line (Neuro-2a), an oligodendrocyte primary culture, and a nonneuronal acute lymphoblastic leukemia cell line (Reh) were used to conduct successful nonradioactive in situ hybridization. Two cDNA probes were used. A 1 kb probe was used to identify the expression of proteolipid protein (PLP) mRNA in a primary culture of oligodendrocytes. A 760 bp cDNA was used to identify the expression of ubiquitin C-terminal hydrolase (UCH-L1) mRNA in Neuro-2a and Reh cells. The probes were labeled with digoxigenin-11-dUTP, denatured, and hybridized with cells fixed on coverslips. The efficiency of the labeling was tested using dot blot analysis by comparing the intensity of our labeled probes with known concentration of the probe labeled by the provider. The nonspecific signals were washed off, followed by detection of a signal specific to the gene. The specificity of the probes was determined by treating the cells with RNase A, hybridizing with bacterial Dig-labeled cDNA (pBR322) and hybridizing the tissues in the absence of labeled probe. During the labeling step, we found that addition of co-precipitants, such as tRNA or glycogen, during precipitation of the labeled probe followed by overnight incubation at -20 C is essential for good recovery of labeled cDNA. Dissolving the labeled probe in a buffer solution containing sodium dodecyl sulfate improves the quantity of the labeling. At the cellular level, prehybridization treatments optimize the permeability of the cell and allow efficient penetration of the labeled probe. Fixing with paraformaldehyde or an ethanol-acetic acid mixture can preserve the structure of cultured cells. To increase the signal to noise ratio, cells were treated with 0.2 N HCl followed by extensive washes using a solution with a high salt concentration and containing dextran sulfate. This treatment significantly improves the signal and reduces the background in cell cultures, but not in tissue sections. The ability to reuse the labeled probe-hybridization mixture is another advantage for using nonradioactive in situ hybridization.

DNA, Complementary↗

PubMed1996

Non-invasive functional mapping with multi-channel near infra-red spectroscopic topography in humans.

Near-infrared spectroscopy (NIRS) is a new technique for non-invasive monitoring of tissue oxygenation and its kinetics. Up to this date, it has been used solely in research for the global hemodynamic change of the brain and for rough regional activation after stimulating the brain physiologically. This paper describes functional brain mapping using multi channel (ten channel) NIRS by applying the motor stimulation in humans. Our results demonstrate that the regional hemodynamic change was detected in a small area around the motor cortex with a time resolution of 1-2 s. NIRS technique offers considerable potential for research and clinical applications with no invasion.

Adult↗

PubMed1996

Bacterial alkaloids mitigate seizure-induced hippocampal damage and spatial memory deficits.

Studies of human patients with temporal lobe epilepsy and animal models of epilepsy have established relationships between seizures, excitotoxic hippocampal damage, and memory impairment. We report that bacterial alkaloids, recently shown to mimic actions of neurotrophic factors in cell culture, attenuate seizure-induced damage to hippocampal neurons and memory impairment in adult rats when administered subcutaneously. Intrahippocampal administration of convulsant doses of kainic acid (KA) to adult rats resulted in degeneration of neurons in CA3, CA1, and hilus. Rats administered KA exhibited (24 h later) deficits in performance on both goal latency and probe trial tasks in Morris water maze (MWM) tests of visuospatial memory. Seizure-induced damage to hippocampal neurons was significantly reduced, to varying extents, in rats administered the bacterial alkaloids K252a, K252b, or staurosporine (daily injections of 4 micrograms/kg body weight) prior to KA administration. The KA-induced deficits in MWM goal latency performance were abrogated in rats administered K252a or K252b, and K252a and staurosporine completely prevented seizure-induced impairment on the MWM probe trial. The alkaloids did not suppress electroencephalographic seizure activity, suggesting a dissociation between synchronization of activity and synaptically mediated excitotoxic injury to hippocampal neurons. Each alkaloid caused an increase in levels of protein tyrosine phosphorylation as determined by Western blot analysis of hippocampal tissue. Our data indicate that these bacterial alkaloids have potent antiexcitotoxic activities which may have clinical utility in epilepsy and other disorders that involve excitotoxic damage.

Alkaloids↗

PubMed1996

Infrared Transitions of H12C14N and H12C15N between 500 and 10 000 cm-1

We have measured the Fourier transform spectrum (FTS) of two isotopomers of hydrogen cyanide (H12C14N and H12C15N) from 500 to 10 000 cm-1. The infrared data have been combined with earlier published microwave and submillimeter-wave measurements. From this analysis new vibration-rotation energy levels and constants are given, based on the observation of a number of new vibrational levels, especially for H12C15N. The Coriolis interaction involving Deltav3 = -1, Deltav2 = 3, and Deltal = ±1 has been observed for a great many levels and in some cases the assignments of laser transitions allowed by this interaction are more clearly shown. New vibration-rotation constants are given that allow one to predict the transition wavenumbers for most of the transitions below 10 000 cm-1 with accuracies of about 0.5 cm-1 or better. Values are given for the power series expansion of the l-type resonance constants and for the centrifugal distortion constants, as well as the usual vibrational and rotational constants.

Journal Article↗

PubMed1996

Pulmonary vasomotor dysfunction is produced with chronically high pulmonary blood flow.

This study examined the hypothesis that chronic high pulmonary blood flow produces dysfunction of the mechanisms of pulmonary vasorelaxation. A 3:1 left-to-right shunt was created in dogs by bilateral femoral artery-femoral vein shunts with use of 6 mm polytetrafluoroethylene grafts. Isolated pulmonary artery rings were studied at the following times: 3 days (n = 2), 2 weeks (n = 4), and 5 months (n = 6). Control animals had no shunt. The following mechanisms of pulmonary vasorelaxation were studied in isolated pulmonary artery rings (4 rings from each dog): (1) endothelium-dependent cyclic guanosine monophosphate-mediated relaxation (response to acetylcholine), (2) endothelium-independent cyclic guanosine monophosphate-mediated relaxation (response to sodium nitroprusside), and (3) beta-adrenergic cyclic adenosine monophosphate-mediated relaxation (response to isoproterenol). Statistical analysis was done by analysis of variance. This model of high pulmonary flow did not produce an increase in pulmonary arterial pressure or transpulmonary gradient. However, chronic high pulmonary flow produced progressive dysfunction of all three of these mechanisms of pulmonary vasorelaxation. By 5 months of high pulmonary flow, acetylcholine produced only 36% +/- 6% relaxation versus 95% +/- 5% in control animals (p < 0.05). Likewise, sodium nitroprusside produced only 69% +/- 6% relaxation versus 100% in control animals (p < 0.05). Finally, isoproterenol produced only 55% +/- 5% relaxation versus 94% +/- 6% in control animals (p < 0.05). We conclude that dysfunction of the mechanisms of pulmonary vasorelaxation may contribute to exaggerated perioperative pulmonary vasoconstriction in the setting of chronic high pulmonary blood flow.

Acetylcholine↗

PubMed1996

Role of ubiquitin carboxyl terminal hydrolase in the differentiation of human acute lymphoblastic leukemia cell line, Reh.

We have previously demonstrated that the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA), induces differentiation of the acute lymphoblastic leukemia cell line, Reh, to a mature non-dividing state. Associated with this differentiation is the expression of ubiquitin carboxyl terminal hydrolase (UCH-L1). To investigate the role of UCH-L1 in TPA-induced Reh differentiation and apoptosis, molecular and chemical inhibition was used. Molecularly, a sequence-specific antisense oligodeoxynucleotide (AODN) directed against UCH-L1 transcript was used to inhibit the expression of the gene. In addition, its complementary sense oligodeoxynucleotide (SODN) was used to indicate the specificity of AODN action. Chemically, sodium borohydride (NaBH4), an inhibitor of UCH-L, was used to block the transcript product. TPA-induced changes in Reh cell growth and morphology, UCH-L1 protein expression, apoptosis contour, surface phenotype, and enzymatic profile were assessed in the presence or absence of NaBH4, AODN or SODN. As previously reported, TPA induced Reh cells to differentiate into monocytoid B lymphocytes and stimulated the apoptotic pathway. However, adding NaBH4 or AODN inhibited the TPA effect on all parameters measured except apoptosis. The sequence in which NaBH4 or AODN were added in relation to TPA did not affect any of the response variables measured. The use of SODN did not influence any of the parameters measured, indicating the specificity of the action. Thus, we conclude that UCH-L1 is involved in the differentiation process of the lymphoblastic leukemia cell line, Reh. Our data suggest that TPA-induced apoptosis of Reh cells has a separate pathway from that of differentiation or that UCH-L1 expression is independent of the apoptotic pathway.

Adolescent↗

PubMed1996

Effect of dolastatin 10 on human non-Hodgkin's lymphoma cell lines.

It is crucial to incorporate new and more potent antineoplastic agents in treating non-Hodgkin's lymphoma since standard chemotherapy fails to cause a significant increase in the survival rate. A potential chemotherapeutic agent is dolastatin 10; hence, the objective of our study is to investigate the effect of the antiproliferative agent dolastatin 10 on different grades of non-Hodgkin's lymphoma cell lines. All cell lines exposed to dolastatin 10 initiated an apoptosis process. Alteration of oncogenes and their product may direct the entry of the cells into apoptosis, among these oncogenes are bcl-2 and c-myc. All cell lines tested expressed c-myc and bcl-2 proteins. However, 24 h after exposing the cell lines to 1 ng/ml dolastatin 10, bcl-2 expression was abolished but there was no significant change in c-myc protein expression. The contradictory roles of c-myc in cell proliferation and death require that other gene(s) products regiment the outcomes of c-myc activity on a cell. A possible candidate for such a modifying gene is bcl-2, whose product prolongs cell survival and blocks apoptosis. Given the above, dolastatin 10 induction of cell arrest is the initiating signal to downregulate the antiapoptotic bcl-2 and reactivate the apoptotic pathway. The reductions in bcl-2 may stabilize the c-myc proliferative action and induce apoptosis.

Antineoplastic Agents↗

PubMed1996

Bryostatin 1 induces ubiquitin COOH-terminal hydrolase in acute lymphoblastic leukemia cells.

It has been previously reported that Bryostatin 1 (Bryo1) induces differentiation of the human acute lymphoblastic leukemia (ALL) cell line, Reh, to a monocytoid B-cell stage. In this study we demonstrate that a novel protein, ubiquitin COOH-terminal hydrolase (UCH-L1), is associated with this differentiation. Reh cells were treated with 200 nmol/l of Bryo1 for 72 h and analyzed for changes in morphology, surface immunophenotype, acid phosphatase and terminal deoxynucleotidyl transferase. Protein patterns of the parent and differentiated cells, by two-dimensional polyacrylamide gel electrophoresis (2D PAGE), were studied. Bryo1-treated cells expressed morphologic, phenotypic and enzymatic features of the monocytoid B-cell stage. The UCH-L1 enzyme (MW-pl 34-5.3) was detected by 2 D PAGE in the differentiated, but not in parent cells. The presence of UCH-L1 in the Bryo1-treated cells was further confirmed by immunoblotting of 2 D PAGE using UCH-L1 polyclonal antibody. Ubiquitin expression was studied in parent and Bryo1-treated cells and was compared with 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated cells. Both agents, TPA and Bryo1, increased the level of ubiquitin expression as detected by flow cytometry. Sodium borohydride, an inhibitor of UCH-L1, inhibited the Bryo1-induced differentiating effect on Reh cells. To date, the mechanism by which Bryo1, exerts its B-cell differentiating effect is not fully understood. This study shows that UCH-L1 expression may play a major role in Bryo1-induced differentiation in pre-B-ALL.

Adolescent↗