An Epistaxis Emergency Associated with Multiple Pollutants in Elementary Students / 生物医学与环境科学（英文）

Emergencies of epistaxis in students caused by environmental pollution have rarely been reported to date. This study aimed to explore the cause of an emergency of epistaxis in elementary students by using a field epidemiological investigation. Twenty-two epistaxis cases from a single school with differences in gender, age, and classroom, were diagnosed within a period of 7 days. The air concentration of chromic acid mist (Cr6+) in the electroplating factory area, new campus, and residential area exceeded the limit of uncontrolled emissions. The emission of HCL and H2SO4 was also observed. Formaldehyde levels in the classrooms exceeded the limits of indoor air quality. Abnormal nasal mucosa was significantly more frequent in the case group (93.3%) and control group 1 (of the same school) (66.7%) than in control group 2 (from a mountainous area with no industrial zone) (34.8%; P < 0.05 and P < 0.01, respectively). On the basis of the pre-existing local nasal mucosal lesions, excessive chromic acid mist in the school's surrounding areas and formaldehyde in the classrooms were considered to have acutely irritated the nasal mucosa, causing epistaxis. Several lessons regarding factory site selection, eradication of chemical emissions, and indoor air quality in newly decorated classrooms, should be learned from this emergency.

Therapeutic Efficacy of VICP+L-ASP/TKI on Adult Patients with B-ALL / 中国实验血液学杂志

<p><b>OBJECTIVE</b>To evaluate the therapeutic efficacy of VICP+L-ASP/TKI on adult patients with B-ALL and to explore the influence factors.</p><p><b>METHODS</b>Forty-one adult B-ALL patients treated with VICP+L-ASP/TKI from August 2008 to June 2014 were following-up. The complete remission(CR) rate, toxicity, overall survival(OS) and event free survival(EFS) after induction treatment were analyzed, the therapeutic outcome of patients between different risk stratification subgroups was compared, the influence of standardized consolidatory and maintaining treatment as well as allogeneic hematopoietic stem cell transplantation(allo-HSCT) on survival time was analyzed.</p><p><b>RESULTS</b>The early death not occurred in 41 patients with B-ALL including 37 cases with CR; the CR rate of 1 course treatment was 90.2%. The follow-up time lasted to March 17, 2015, the median follow-up time was 25(9-79) months; the 1 year OS rate was 75.3%, the EFS rate was 58.3%. Analysis of risk factors showed that the initial WBC count over 30×10/L, LDH over 250 U/L and minimal residual disease(MRD) over 10after treatment were poor prognostic factors. After remission, the standardized consolidatory treatment or allo-HSCT according to the "2012 China adult ALL diagnosis and treatment expert consensus" could improve long-term survival, 3 years OS rate was 73.8% and 61.5% respectively, 3 years EFS were 63.5% and 65.7% respectively. The main toxic and side effects were hematologic reactions, the hematologic adverse reaction of IV grade was observed in 97.6%(40/41) during induction treatment.</p><p><b>CONCLUSION</b>Induction chemotherapy based on VICP+L-ASP/TKI and standardized consolidatory after remission according to the "2012 China adult acute lymphoblastic leukemia diagnosis and treatment expert consensus" can improve the therapeutic efficacy. The allo-HSCT should be actively performed for B-ALL paients with high risk(elevated initial WBC count and LDH level); at some time, the regularly monitoring MRD and adjusting therapeutic protocol according to monitoring result can promote the prognosis of adult B-ALL patients.</p>

Efficacy and safety of the HAA regimen as induction chemotherapy in 236 de novo acute myeloid leukemia / 中华血液学杂志

<p><b>OBJECTIVE</b>To evaluate the efficacy and safety of the HAA regimen (homoharringtonine, cytarabine and aclarubicin) as induction chemotherapy in de novo acute myeloid leukemia (AML).</p><p><b>METHODS</b>The efficacy and safety of 236 de novo AML patients who received the HAA regimen as induction chemotherapy were retrospectively analyzed. The complete remission (CR) rate was assayed. Kaplan-Meier method was used to estimate overall survival (OS) and relapse free survival (RFS), and the differences were compared by Log-rank test.</p><p><b>RESULTS</b>The overall CR rate was 78.0%, and 65.7% of the patients attained CR in the first induction cycle. The early death rate was 4.7%. The median followup time was 41(1-161) months. The estimated 5-year OS and 5-year RFS rates were 44.9% and 45.5%, respectively. The CR rates of patients with favorable, intermediate and unfavorable cytogenetics were 92.9%,78.6%and 41.7%, respectively. The 5-year OS of favorable and intermediate group were 61.1% and 45.1%, respectively. The 5- year RFS of favorable and intermediate group were 49.0% and 45.4%, respectively. The median survival time of unfavorable group was only 5 months. The side effects associated with the HAA regimen were tolerable, in which the most common toxicities were myelosuppression and infection.</p><p><b>CONCLUSION</b>The HAA regimen is associated with a higher rate of CR and longer survival time and its toxicity could be tolerated.</p>

HAA regimen as induction chemotherapy for newly diagnosed acute myelogenous leukemia / 中华血液学杂志

<p><b>OBJECTIVE</b>To analyse the outcome of newly diagnosed adult acute myeloid leukemia (AML) patients treated with HAA (homoharringtonine, cytarabine and aclarubicin) regimen and explore the efficacy and safety of this regimen.</p><p><b>METHODS</b>Eighty patients were treated with HAA regimen. The complete remission (CR) rate was observed. Kaplan-Meier method was used to estimate relapse free survival (RFS) rate and the differences were compared with 2-sided log-rank test.</p><p><b>RESULTS</b>Of the 80 patients, 65 (81%) attained CR and the CR rate after the first course of induction was 75%. For the CR patients, the median follow-up was 26 (2 -69) months, and the estimated 3-year overall survival (OS) rate was 51% and the estimated 3-year RFS was 53%. For the AML-M5 and AML-M /M2 patients the CR rate was 74% and 87% and 3 year RFS of CR patients was 75% and 37%, respectively. The CR rate of 100%, 83% and 20% was achieved in patients with favorable, intermediate and unfavorable cytogenetics, respectively. The 3 year OS for favorable and intermediate group was 76% and 50% respectively. The median survival time of unfavorable group was only 6 months.</p><p><b>CONCLUSION</b>HAA regimen is a safe, efficacious, and well-tolerable induction therapy for newly diagnosed AML.</p>

Clinical study of amphotericin B in the treatment of invasive fungal infection in 111 hematological disorder patients with neutrocytopenia / 中华血液学杂志

<p><b>OBJECTIVE</b>To compare the differences in clinical therapeutic effect and safety between amphotericin B and its liposome form in treating invasive fungal infection (IFI) in hematological disorder with neutrocytopenia.</p><p><b>METHODS</b>Of 111 patients with IFI, 82 were treated with amphotericin B and 29 with amphotericin B liposome. The mean cumulative dose of amphotericin B was 617 (60-1895) mg and the mean course was 18 (7-60) d, and those for amphotericin B liposome was 925 (140-3420) mg and 13 (7-50) d, respectively.</p><p><b>RESULTS</b>The total effective rates of amphotericin B and its liposome groups were 69% and 58%, respectively (P>0.05). The adverse effect rates of chill and fever in amphotericin B and its liposome groups were 21% and 10% (P>0.05), hypopotassemia 34% and 14% (P=0.03), hepatic impairment 22% and 17% (P>0.05), and renal impairment 9% and 3%, respectively (P>0.05).</p><p><b>CONCLUSION</b>The therapeutic effect for IFI of amphotericin B and its liposome was similar. The severe adverse reaction of amphotericin B liposome was slightly lower than that of amphotericin B.</p>

Induction of apoptosis by homoharringtonine in G1 phase human chronic myeloid leukemic cells / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Homoharringtonine (HHT) is a cephalotaxine ester derived from an evergreen tree found wildely throughout southern China, which has antileukemic activities against a variety of acute myeloid leukemic cells. For the sake of illustrating the mechanisms of HHT in the treatment of leukemia, we assessed the effect of HHT on the apoptosis of human chronic myeloid leukemic cell line K562.</p><p><b>METHODS</b>The apoptosis of K562 cells induced by HHT was analyzed by transmission electron microscopy, agarose gel electrophoresis of DNA, flow cytometry and terminal deoxyribonucleotidyl transferase-mediated dUTP-biotin nick labeling.</p><p><b>RESULTS</b>Characteristic apoptosis-related features emerged in K562 cells after exposed to HHT at a concentration 0.05-100 microg/ml. Transmission electron microscopy of HHT treated K562 cells displayed chromatin condensation and aggregation under the nuclear membrane, nuclear fragmentation and apoptosis body formation. Typical DNA ladder in agarose gel electrophoresis was observed in the cells exposed to HHT. The cell cycle analysis measured by flow cytometry showed G1 phase cells decreased with the increase of S phase cells while apoptosis was induced by HHT in K562 cells. The percentage of apoptotic cells in K562 cells treated with 50 microg/ml of HHT decreased significantly when pretreated with 1 microg/ml of cycloheximide, 0.05 microg/ml of Actinomycin D respectively.</p><p><b>CONCLUSIONS</b>HHT has apoptotic effects on K562 cells. The HHT induced apoptosis mainly of the cells in G1 phase and this process required RNA transcription and protein synthesis.</p>

Cytogenetic and clinical analysis of -7/7q- abnormalities in acute leukemia and myelodysplastic syndrome / 中国实验血液学杂志

The objective was to study the incidence and prognosis significance of -7/7q- abnormalities in acute leukemia and myelodysplastic syndrome. Conventional cytogenetic analysis of R-band was used to test -7/7q- chromosome abnormalities in 410 patients with acute leukemia (AL), in 71 cases of myelodysplastic syndrome (MDS) and in 36 cases of chronic myelogenous leukemia in accelerated phase (CML-AP). The results showed that the incidences of -7/7q- abnormalities in AL, MDS and CML-AP patients were 4.88%, 9.86% and 8.33% respectively. The -7/7q- abnormalities could be found in acute myeloblastic leukemia (AML) and acute lymphocytic leukemia (ALL), incidences of which were 4.70% and 6.25% (P > 0.05) respectively. 9 cases had -7 or 7q- as the sole chromosome abnormalities, 22 cases showed other additional chromosome abnormalities: -X, -5, +8, t(3; 3), t(11;16) and t(2;11). Monosomy -7 and 7q- abnormality clone was found in one patient with MDS-RAEB, and the number of cells with -7 abnormality was greater than that of 7q- abnormality cells. Four patients acquired CR among 7 patients with ALL after chemotherapy, but 2 out of 13 patients with AML achieved CR while 6 out of 7 patients with MDS transformed into AL. No patients with CML-AP achieved CR. In conclusion, -7/7q- is a frequent aberration in hematologic malignancies as well as AML and ALL. The monosomy -7 and 7q-abnormalities were detected in the same patient. The patients with -7/7q- abnormalities show poor prognosis.

Mechanisms of inhibitory effect of Ubenimex on human leukemic cells / 浙江大学学报·医学版

OBJECTIVE: To study the mechanism of inhibitory effect of Ubenimex on human leukemic cells. METHODS: K562 and HL60 cells were treated with Ubenimex at different concentrations, and the growth inhibition was analysed by MTT assay. Cell apoptosis was evaluated by light microscopy, agrose gel electrophoresis, TUNEL labeling method and flow cytometry (FCM) assay. RESULTS: (1)Treatment with Ubenimex remarkably inhibited the growth of HL60 cells, the IC(50) of Ubenimex for HL60 cells was 13.03&mgr;g/ml. But K562 cells were less sensitive than HL60. Ubenimex inhibited the growth of HL60 and K562 cells in a dose-dependent manner. (2)Apoptosis of leukemic cells was induced by Ubenimex, which was shown by the changes in morphology, DNA ladder on agrose gel, TUNEL labeling,typical peak before G1 phase of cell cycle and the positive of Annexin V(FITC) on the cells membrane with FCM. (3)Ubenimex induced apoptosis of K562 and HL60 cells in a dose-and-time-dependent manner. (4)The cell cycle analysis by FCM showed that the HL60 cells were blocked in G1 phase after treated by Ubenimex. Conclution Ubenimex can efficiently induce apoptosis of HL60 and K562 cells, this may be one of the mechanisms for inhibiting effect of Ubenimex on leukemia.