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Biomedical subjects

Ran Meng

Publications and source records attributed to Ran Meng.

14 recordsLinked to original sources
PubMed2006

Dynamic change of coagulation and anticoagulation markers of patients with acute cerebral infarction during intravenous urokinase thrombolysis.

BACKGROUND AND OBJECTIVE: The variations of blood coagulation and anticoagulation are of clinical importance in patients with acute cerebral infarction during intravenous urokinase (UK) thrombolysis. Although intravenous heparin is commonly used after thrombolytic therapy, few reports have addressed the relationship between the degree of anticoagulation and clinical outcomes, specifically the effect of thrombolytic agents on hemostasis. In this study, we dynamically monitored the activated partial thromboplastin time (APTT), the prothrombin time (PT), the thrombin time (TT) and the activated partial thromboplasmin time (APTT) in 56 patients with acute cerebral infarction during intravenous urokinase thrombolysis and analysed the relationship among the blood coagulation biomarkers (APTT, PT, TT, AT-III), as well as baseline patient characteristics and clinical outcomes. This allowed us to explore the valuable biomarkers for securing the thrombolysis regimen in clinical practice. METHODS: The levels of PT, APTT, TT and AT-III in peripheral blood of 56 patients with acute cerebral infarction and 50 normal controls were assayed by ELISA. Dynamic transformation of these markers at the baseline and the time points of the first, second, fourth, eighth, 12th, 24th, 48th, 72nd and 96th hour after intravenous UK thrombolysis was monitored serially. The relationship between the levels of these biomarkers and the clinical effectiveness and safety of urokinase thrombolysis was evaluated. RESULTS: The levels of PT, APTT, TT and AT-III in patients before intravenous UK thrombolysis were significantly lower than those in age- and sex-matched normal controls (all p<0.05). After treatment with UK, the levels of PT and APTT rose quickly during the first 4 hours (all p< 0.05), and then gradually recovered, reaching baseline at about the 48th hour. The activity of AT-III was slightly increased and showed fluctuations after UK infusion (p< 0.05), however the fluctuated range was not remarkable and lacked specificity. CONCLUSIONS: Dynamic monitoring of PT, APTT and TT can indicate coagulative and anticoagulative functions of patients with acute cerebral infarction during intravenous urokinase thrombolysis. Monitoring of these markers can be helpful both in regulating the infusion speed and the dosage of UK, as well as increasing the efficacy and safety of UK therapy. However, assay for AT-III might be unnecessary.

Aged↗
PubMed2006

[The diagnosis and treatment of polycythemia rubra vera manifesting as acute cerebral stroke].

OBJECTIVE: To analyze the particularities of diagnosis and treatment of acute cerebral stroke secondary to polycythemia vera (PV). METHODS: To track and evaluate the clinical parameters, the manifestations of CT/MRI, the data of laboratory examinations, the therapeutic responses and the prognosis of acute cerebral stroke secondary to PV. Twenty-two cases of PV with initial presentation as acute stroke were analyzed. RESULTS: (1) 55.0% of the patients with stroke as the initial presentation of to PV had multiple lacuna infarction. (2) 37.5% of the patients had a temporary symptom aggravation after receiving a therapeutic regimen of blood-letting and chemotherapy, whereas, the stroke symptoms improved and became stable when treated with blood-letting combined with hemodilution and chemotherapy simultaneously. (3) Six cases received homoharringtonine treatment and all of them reached complete remission (CR). However, 3 of them showed ST segment and T-wave changes in electrocardiogram and 2 of them had bone marrow depression. Four cases received arsenic trioxide and obtained CR, but the relapse rate reached 50.0%. Nine cases were treated with hydroxycarbamide and all of them obtained CR. CONCLUSIONS: (1) Stroke secondary to PV should be treated with stroke regimen as well as PV therapy, and hydroxycarbamide might have stable benefit and few side effects. (2) Hematocrit assay should be used as a routine item in stroke patients with frequently relapsed.

Adult↗
PubMed2006

Effects of arsenic trioxide administration styles on leukocytosis.

OBJECTIVE: To study the effects of constantly slow intravenous arsenic trioxide (As2O3) infusion regimen on decreasing leukocytosis in vivo and in vitro. METHODS: Three kinds of leukemia cells, NB4, K562, and acute promyelocytic leukemia (APL) cells, were cultured in the media with constant concentration and varying concentrations of As2O3 respectively for 24 hours. Seventy-five patients were enrolled in two groups randomly. In trial group, 37 patients received continuously slow intravenous As2O3 infusion regimen for 24 hours with an infusion rate of 8 drips per minute and total infusion duration of about 18-21 hours daily. In control group, 38 patients received routine regimen with an infusion rate of 45-55 drips per minute and total infusion duration of about 2-3 hours daily for 24 hours. The daily As2O3 dosage was 0. 16 mg/kg. The intracellular arsenic concentration was measured by atomic fluorescence assay. The apoptosis rate of cells, CD33- CD11b+ cells, and CD33+ CD11b- cells were monitored by flow cytometry. RESULTS: The apoptosis rates of NB4, K562, and APL leukemia cells in the media with constant As2O3 concentration were 56.6% +/- 2.4%, 27.6% +/- 3.1%, and 52.2% +/- 2.8%, respectively, which were significantly higher than those with changing As2O3 concentration (23.2% +/- 2.1%, 11.0% +/- 2.5%, and 21.0% +/- 2.5%, respectively, P < 0.01). The apoptosis rates of APL, M2 type acute myeloid leukemia (AML-M2), and chronic myeloid leukemia (CML) patients in the trial group (28.5% +/- 1.9%, 9.5% +/- 0.6%, and 12.5% +/- 1.8%) were also significantly higher than those in control group (8.5% +/- 2.2%, 2. 9% +/- 0.8%, and 4.5% +/- 1.2%; P < 0.05). The ratios of CD33 CD11b- and CD33- CD11b+ cells in control group were significantly higher than those in trial group. CONCLUSION: The continuously slow intravenous As2O3 infusion regimen can obtain high efficiency of apoptosis and low differentiation proportion, relieve leukocytosis, and gain maximal therapeutic benefit.

Antineoplastic Agents↗
PubMed2005

Effects of administration styles of arsenic trioxide on intracellular arsenic concentration, cell differentiation and apoptosis.

We studied the effects of varying and steady-state concentrations of arsenic trioxide (As2O3) on apoptosis and differentiation of several cell lines in vitro. We also studied the same effects of fluctuating vs constant concentrations of As2O3 in vivo in patients treated with daily 3-hour fast infusions or daily slow, continuous infusions. Intracellular concentrations of arsenic and apoptosis rate were higher whereas differentiation was reduced in cells exposed to constant concentrations of As2O3.

Apoptosis↗
PubMed2004

[Clinical observation and following up of two administration methods of arsenic trioxide in treatment of acute promyelocytic leukemia].

OBJECTIVE: To assess the effectiveness and security of two arsenic trioxide (As(2)O(3)) administration methods in treatment of acute promyelocytic leukemia (APL). METHODS: Forty-eight APL cases were treated with As(2)O(3) with the total daily dosage of 0.16 mg/kg that was divided into two equal doses diluted in 250 ml of 5% glucose given twice in the morning and evening respectively by intravenous infusion' at a speed of 8 drops/min with an interval of 2-3 hours. Forty-eight sex- and age-matched APL cases were treated with As(2)O(3) with the same total daily dosage of 0.16 mg/kg given according to the routine method: infused intravenously once a day with a duration of at most 2 hours. Serum was collected at different time points to examine the arsenic concentration. The remission rate and side effects were observed. RESULTS: The remission rate was 93.8% in the patients treated by the new method, and was 83.3% in the patients treated by the routine method 28 days after the treatment. The lasting duration of effective arsenic level was at least 18.4 +/- 3.3 hours in the new method group, and was 9.4 +/- 1.6 hours in the routine method group. The average time from the initiation of treatment to complete remission (CR) in the new method group was 26.4 +/- 2.4 days, and was 35.7 +/- 4.8 days in the routine method group. No late liver functional lesion and bone marrow depression was found in the two groups during the 6 months followed up. CONCLUSION: The 'multi-times and slowing intravenous infusion' method relieves the side effects of As(2)O(3) treatment, increases the CR rate in treatment of APL.

Adolescent↗
PubMed2004

[Clinical and experimental study of cardiac effects of conventional dosage arsenic trioxide in APL patients].

OBJECTIVE: To investigate cardiac effects of arsenic trioxide (As(2)O(3)) at conventional dosage in acute promyelocytic leukemia (APL) patients. METHODS: The basical heart rate, electrocardiograph, plasma As(2)O(3) concentration of APL patients were dynamically monitored. The action potential duration and current of I(Ca-L) in guinea pig cardiac ventricular myocytes were assayed by patch clamp technique, and the elevated cytosolic [Ca(2+)]i of guinea pig ventricular myocytes induced by As(2)O(3) by laser confocal microscopy. RESULTS: Approximately 52.5% - 35% of 40 APL patients manifested poor cardiac effects of different degree when As(2)O(3) intravenous infused at conventional doses in the initial 1 or 2 weeks with fast heart rate or prolonged QT interval. As(2)O(3) at concentration of 1, 2, 5 micro mol/L prolonged action potential duration from (563.0 +/- 55.8) ms to (737.7 +/- 131.7), (842.4 +/- 115.6) and (1103.2 +/- 96.3) ms respectively (P < 0.05, P < 0.01, P < 0.01), and increased I(Ca-L) of guinea pig cardiac ventricular myocytes as well as the respectively cytosolic [Ca(2+)]i. Calcium channel blocking agent can cut-out the effect. CONCLUSION: As(2)O(3) intravenous infusion at conventional doses can cause tachycardia and prolong QT interval. The probable mechanism might be that As(2)O(3) affects the ion channels and cytosolic calcium.

Adult↗
PubMed2004

[Association between subacute combined degeneration, vitamin B12 deficiency and megaloblastic anemia].

OBJECTIVE: To investigate the association between subacute combined degeneration (SCD) and vitamin B(12) (VB(12)) deficiency and megaloblastic anemia (MA). METHODS: The serum level of VB(12), severity of anemia and lesions in CNS were analysed in 36 cases diagnosed as SCD. In addition, MRI neuro-electrophysiologic examination and CSF myelin basic protein (MBP) concentration were monitored dynamically. The prognosis of SCD was evaluated in relation to the time of the initiation of therapy. RESULTS: Average ferrohemoglobin level in patients was (77.1 +/- 11.2) g/L and the average blood serum level of VB(12) was (87.0 +/- 21.4) ng/L before treatment with an abnormality rate of 47.2%. However, there was no linear correlation between the severity of lesions in CNS and ferrohemoglobin level or level of serum VB(12) (correlation coefficient: r = -0.1917, 0.0926, P > 0.5; r = 0.207, 0.101, P > 0.5, respectively). The comprehensive abnormal rate of evoked potential was 100%, which might occur prior to the clinical symptoms of SCD. The abnormal rate of MRI was 71.4%, and some lesions could diminish or disappear after treatment. The MBP levels in CSF were (3.96 +/- 1.66) ng/L, and (2.25 +/- 1.66) ng/L before and 3 months after the treatment. No significant improvement of symptoms and signs were seen when the treatment was initiated 6 months after the diagnosis. CONCLUSION: SCD is associated with VB(12) deficiency and often accompanied by MA, but there is no linear correlation. Lesions of SCD in spinal cord or brain can be demonstrated in MRI. Evoked potential is critical for early diagnose and identification of silent cases of SCD. The level of MBP in CSF can reflect the severity of the lesion and prosthetic state of myelin sheath. Early diagnosis and treatment play an important role in decreasing the degree of the permanent dysfunction of CNS in SCD.

Adolescent↗
PubMed2004

[Effects of protein tyrosine kinase, protein tyrosine phosphatase and protein kinase C on the apoptosis of arsenic trioxide treated NB4 cells and human cortex neurons].

OBJECTIVE: To investigate the effects of protein tyrosine kinase (PTK), protein tyrosine phosphatase (PTP) and protein kinase C (PKC) on apoptosis and observe the changes of cytosolic calcium ([Ca(2+)]i) of arsenic trioxide (As2O3) treated human leukemia cells NB4 and cortex neurons. METHODS: [Ca(2+)]i of NB4 cells and cortex neurons was probed with Fluo-3/AM, its changes were assayed with laser confocal microscopy in real-time after As2O3 treatment at different concentrations, the effects of PTK and PTP and the activation of PKC on these changes with confocal microscopy and phosphorus radioisotope assay. DNA ladders of NB4 cells and cortex neurons after exposed to As2O3 were observed. RESULTS: As2O3 at 1 micromol/L could remarkably increase the [Ca(2+)]i of NB4 cells but had no effects on neurons. Vanadate, a kind of PTP inhibitor, could promote the increase of [Ca(2+)]i treated by 2, 5, 10 micromol/L As2O3 in a dose-dependent manner. The mean total increase rates at 240 seconds after exposed to As2O3 at different concentrations were (6.5 +/- 2.3)%, (21.7 +/- 2.1)%, (49.2 +/- 2.5)% for NB4 cells, and (6.7 +/- 2.1)%, (19.4 +/- 2.5)%, (52.3 +/- 2.7)% for cortex neurons, respectively. Genistein, a kind of PTK inhibitor, could decrease the increase of [Ca(2+)]i treated by 2, 5, 10 micromol/L As2O3 in a dose-dependent manner. The mean total inhibited rates at 240 seconds after As2O3 treatment at different concentrations were (6.7 +/- 2.9)%, (25.6 +/- 2.5)%, (52.2 +/- 3.5)% for NB4 cells, and (7.8 +/- 3.1)%, (18.1 +/- 2.8)%, (51.3 +/- 3.3)% for cortex neurons, respectively. The activation of PKC began to increase as exposed to As2O3 at 1 micromol/L for 3 h, and kept rising continuously in NB4 cells and at 24 h DNA ladders emerged. However, none of the above results was found in human cortex neurons, but when exposed to 2 micromol/L As2O3, the activation of PKC and DNA ladders did emerge in neurons. CONCLUSIONS: The phosphorylation and dephosphorylation of PTK and PTP participated in nonspecific apoptosis signal transduction pathway related to As2O3, and accompanied with PKC activation. The [Ca(2+)]i elevation was closely related to increased PKC activation. There existed difference in dose tolerances to As2O3 between NB4 cell and cortex neurons.

Adult↗
PubMed2003

[Study on cardiac toxicity in acute promyelocyte leukemia treatment of arsenic trioxide intravenous infusion in general dose].

OBJECTIVE: To study the cardiac toxicity of arsenic trioxide (As(2)O(3)). METHODS: To investigate and analyze the probable mechanisms of cardiac toxicity of As(2)O(3) by dynamic monitoring of clinical manifestations, basal cardiac rate and electrocardiographic data of acute promyelocyte leukemia (APL) patients during As(2)O(3) therapy. The instant change of the action potential, the I(Ca-L) and I(k) of single cardiac myocyte of guinea pig was also observed with patch clamp dynamically. RESULTS: Approximately 71.4% of the 28 cases of APL showed cardiac toxic reaction in different degree in the first week after As(2)O(3) intravenous infusion in general dose, mainly expressing rapid heart rate or prolonged QT interval. As(2)O(3) could prolong the action potential duration from (563.0 +/- 55.8) ms to (737.7 +/- 131.7) ms (P < 0.05) and increased the I(Ca-L) and I(k) of single cardiac myocyte of guinea pig in vitro. CONCLUSION: As(2)O(3) intravenous infusion in general therapeutic dose can cause tachycardia and prolong QT interval in some of the APL patients. The probable mechanism of these side-effects may be due to instant involvement of ionic channel of cardiac myocyte.

Adult↗
PubMed2003

The effect of arsenic trioxide on QT interval prolongation during APL therapy.

OBJECTIVE: To investigate the cardiac effect of QT interval prolongation in the treatment of acute promyelocytic leukemia (APL) with arsenic trioxide (As(2)O(3)), and the relationship between QT and serum arsenic concentration. METHODS: Blood serum arsenic concentrations of thirty APL patients were determined at 2 hours, 4 hours, 8 hours, and 24 hours after As(2)O(3) injection using atomic fluorophotometry. Cardiac functions were measured simultaneously using a 12-lead body-surface electrocardiogram (ECG). Q-T intervals were manually measured, and then corrected using Bazett's formula (QTc). QT dispersion (QTd) was also calculated. In order to assess the effects of arsenic on the symptoms of anemia, twenty-four anemia patients were divided into two groups on the basis hemoglobin concentration: Group 1 (Hb > or = 90 g/L), and Group 2 (60 g/L < or = Hb < 90 g/L). QTc and QTd of these patients were also manually measured. RESULTS: All QT intervals of APL patients treated with As(2)O(3) injection were prolonged [32.2 ms (27, 41 ms); P < 0.05], but the changes of QTd were not prominent [3 ms (-8, 7 ms), P > 0.05]. There was a delay of 2 hours in maximum QTc following peaks in serum arsenic concentration. Changes in QTc and QTd of the two anemic groups were not prominent. CONCLUSIONS: As(2)O(3) can prolong QTc intervals in APL patients, but the effects are delayed compared to peak serum arsenic concentrations. As(2)O(3) has no prolongation effect on QTd. Mild and moderate anemia do not effect QTc and QTd.

Arsenic Trioxide↗