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1.
Journal of Experimental Hematology ; (6): 1816-1821, 2018.
Article in Chinese | WPRIM | ID: wpr-774380

ABSTRACT

OBJECTIVE@#To explore the clinical efficacy and safety of unrelated umbilical cord blood transplantation (UCBT) for the treatment of Wiskott-Aldrich syndrome(WAS).@*METHODS@#Five pediatric patients with WAS received single UCBT were retrospectively analyzed. The median age of these male patients was 268 days (range, 3 days -695 days). Among them, 2 patients were transplanted with a 6/6 matched cord blood graft,the other 3 patients received a 5/6 matched cord blood graft. Myeloablative conditioning regimen was applied, and all patients received a combination of cyclosporine and mycophenolate mofetil for the prophylaxis of graft versus host disease (GVHD). The recovery time of neutrophils and platelets as well as chimerism after transplantation were taken as the evidence of hematopoietic reconstruction.@*RESULTS@#All the five pediatric patients had hematopoietic recovery. A median time of neutrophil cells after transplantation was at 15.8 days (range,11 days -25 days), and platelet recovery was at a median of 20.4 days(range,12 days-30 days). Chimerism data were available for 5 patients at 30 days after UCBT, 4 out of the 5 patients had full donor chimerism and only one patient had mixed chimerism. There were 2 cases with pre-engraftment syndrome, 3 cases with acute GVHD gradeⅠ-Ⅲ, 4 cases with pulmonary infection and cytomegalovirus infection, but chronic GVHD was not observed in 5 cases. Four patients were alive with a median follow-up of 12.3 months (range, 5 months-17 months), and one patient had died at 22 days after UCBT.@*CONCLUSION@#Unrelated umbilical cord blood transplantation is a safe and effective treatment method for Wiskott-Aldrich syndrome.


Subject(s)
Humans , Infant , Infant, Newborn , Male , Cord Blood Stem Cell Transplantation , Graft vs Host Disease , Retrospective Studies , Transplantation Conditioning , Treatment Outcome , Wiskott-Aldrich Syndrome
2.
Journal of Southern Medical University ; (12): 113-116, 2015.
Article in Chinese | WPRIM | ID: wpr-239236

ABSTRACT

<p><b>OBJECTIVE</b>To explore the protective effects of rutin against learning and memory impairment induced by trimethyltin (TMT) and investigate the possible mechanism.</p><p><b>METHODS</b>Forty 6- to 9-week-old male BALB/c mice were randomized equally into saline group (control), TMT group, TMT+rutin group, and rutin group. Mouse models of learning and memory impairment were establish by acute TMT (2.25 mg/kg) exposure. In TMT+rutin and rutin treatment groups, the mice received intraperitioneal injection of rutin (10 mg/kg) for 1 week before TMT exposure. Twenty-four hours after TMT exposure, Morris water maze test was employed to test the escape latency of the mice, and the synaptophysin expression in the hippocampus and cortex were analyzed by Western blotting.</p><p><b>RESULTS</b>Compared that in TMT group, the escape latency of the mice in water maze test was significantly shorter in the other 3 groups (P<0.05); the escape latency in TMT +rutin group was similar with that in the control and rutin groups (P>0.05). Western blotting showed significantly decreased synaptophysin expression in the hippocampus and cortex in TMT group (P<0.05); synaptophysin expression in TMT +rutin group increased significantly compared with that in TMT group (P<0.05) but showed no statistical significance from that in rutin and control groups (P>0.05).</p><p><b>CONCLUSION</b>Rutin pretreatment offers protective effect against TMT-induced learning and memory impairment in mice possibly by antagonizing decreased synaptophysin in the hippocampus and cortex.</p>


Subject(s)
Animals , Male , Mice , Cerebral Cortex , Metabolism , Hippocampus , Metabolism , Learning , Memory Disorders , Drug Therapy , Mice, Inbred BALB C , Neuroprotective Agents , Pharmacology , Rutin , Pharmacology , Synaptophysin , Metabolism , Trimethyltin Compounds
3.
Journal of Experimental Hematology ; (6): 1621-1623, 2014.
Article in Chinese | WPRIM | ID: wpr-340448

ABSTRACT

This study was aimed to investigate the clinical efficacy of idarubicin combined with methotrexate for treatment of patients with central nervous system diffuse large B-cell lymphoma. A total of 88 patients with central nervous system diffuse large B-cell lymphoma was selected, out of them 54 patients received idarubicin combined with methotrexate and were selected as A group, other 34 patients received only methotrexate and were selected as B group (control group). Clinical efficacy and safety were compared after treatment. The results showed that in A group 84 patients achieved complete remission (CR), 5 patients archived partial remission (PR), the total remission rate of A group was 72.2%; in B group 10 patients achieved complete remission (CR), 4 patients archived partial remission (PR), the total remission rate of B group was 41.2%; the average survival time of A group was 33.172 months, and the average survival time of B group was 26.305 months, the former was significantly higher than latter (P < 0.05). It is concluded that idarubicin combined with methotrexate for the patients with central nervous system diffuse large B-cell lymphoma is effective and safe, and may be used in clinic.


Subject(s)
Humans , Antineoplastic Combined Chemotherapy Protocols , Therapeutic Uses , Central Nervous System Neoplasms , Drug Therapy , Idarubicin , Lymphoma, Large B-Cell, Diffuse , Drug Therapy , Methotrexate , Remission Induction , Treatment Outcome
4.
Chinese Journal of Applied Physiology ; (6): 346-350, 2013.
Article in Chinese | WPRIM | ID: wpr-235362

ABSTRACT

<p><b>OBJECTIVE</b>To observe the neurologic damage in rat hippocampus after electromagnetic field (EMF) acute or chronic irradiation and research the protective effects of Chinese medicine diet (CMD) which comprised ferulic acid, ginsenoside, astragalus polysaccharide and rhodiola sachalinensis.</p><p><b>METHODS</b>Eighty rats were divided into ten groups (n = 8): normal diet with shame irradiation group (NS), normal diet with chronic irradiation group (NCI), three groups of normal diet with acute irradiation after 3 h, 24 h, 72 h (NAI), Chinese medicine diet with shame irradiation group (CS), Chinese medicine diet with chronic irradiation group (CCI), three groups of Chinese medicine diet with acute irradiation after 3 h, 24 h, 72 h (CAI). The chronic EMF irradiation were performed by electromagnetic wave at 15 W/cm2 for 20 min everyday for 8 weeks continuously. The acute EMF irradiation were performed by electromagnetic wave at 65 W/cm2 for 20 min after feeding with CMD for 8 weeks. The learning and memory were evaluated by Morris water maze before/after electromagnetic wave irradiation. The apoptotic cells in hippocampus was detected by Tunel staining. The peroxidation damage of EMF and the protective effect of CMD intervention were assayed by measuring superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px) and reactive oxygen species (ROS).</p><p><b>RESULTS</b>The acute and chronic EMF irradiation disturbed the ability of learning and memory significantly (P < 0.05), CMD intervention markedly antagonized this effect. The apoptotic cells in hippocampus increased evidently after EMF irradiation (P < 0.05), but CMD intervention reduced the apoptotic cells. The acute and chronic EMF irradiation induced the oxidative stress by down-regulating SOD activity, GSH-Px activity, ROS inhibiting and up-regulating the content of MDA obviously (P < 0.05), and CMD intervention reduced peroxidation damage significantly (P < 0.05).</p><p><b>CONCLUSION</b>The acute and chronic EMF irradiation could initiate neurologic damage in hippocampus. CMD intervention has protective effect on the impaired learning and memory, the neuron apoptosis, the peroxidation damage induced by EMF irradiation. CMD intervention plays a significant protective role in antagonizing neurologic damage in the later stage of acute irradiation and chronic irradiation.</p>


Subject(s)
Animals , Female , Male , Rats , Apoptosis , Drugs, Chinese Herbal , Therapeutic Uses , Electromagnetic Fields , Hippocampus , Radiation Effects , Oxidation-Reduction , Oxidative Stress , Phytotherapy , Radiation Injuries, Experimental , Drug Therapy , Reactive Oxygen Species
5.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 172-177, 2012.
Article in Chinese | WPRIM | ID: wpr-273532

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the injury effects of microwave on the visual performance and the apoptosis of retinal ganglion cells (RGCs) in rats and the relationship between the impaired visual performance and RGCs apoptosis induced by microwave.</p><p><b>METHODS</b>The visual performance of rats was observed by Electroretinogram (ERG) and Flash visual evoked potentials (F-VEP). The apoptosis of RGCs in vivo and in vitro was detected by TUNEL assay and Hoechst staining.</p><p><b>RESULTS</b>Microwave exposure had no influence on ERG-a wave. The amplitude of ERG-b wave decreased significantly on the 3rd day and 7th day after microwave exposure (P < 0.01).The latency of ERG-b wave shortened significantly only at 3rd day after microwave exposure (P < 0.01). The latency of F-VEP extended markedly on the 3rd day after exposure (P < 0.05) and recovered on the 7th day after microwave exposure. The amplitude of F-VEP decreased significantly in exposure group, as compared with sham-exposure group, on the 3rd day and 7th day after microwave exposure (P < 0.05). After microwave exposure for 12 h, the apoptotic rate of RGCs in rat increased from 2.85% to 6.73%, and on the 7th day after exposure, the apoptotic rate of RGCs remained 8.93% (P < 0.05). The apoptotic rate of cultured RGCs increased from 8.42% to 13.91% at 6 hour (P < 0.05) and to 24.14% at 24 hour (P < 0.01) after microwave exposure (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>Microwave exposure can injure the visual performance of rats, and the apoptosis of RGCs induced microwave may be one of the main pathological mechanisms.</p>


Subject(s)
Animals , Male , Rats , Apoptosis , Radiation Effects , Cells, Cultured , Microwaves , Rats, Sprague-Dawley , Retina , Radiation Effects , Retinal Ganglion Cells , Pathology , Radiation Effects
6.
Chinese Journal of Hematology ; (12): 830-835, 2011.
Article in Chinese | WPRIM | ID: wpr-345977

ABSTRACT

<p><b>OBJECTIVE</b>To explore the relationship of clinical features, therapeutic measures, laboratory findings, the origin of tumor cells as well as prognosis in Chinese patients with diffuse large B-cell lymphoma (DLBCL).</p><p><b>METHODS</b>One hundred and six patients with DLBCL were retrospectively assayed and followed up, the international prognostic index (IPI) score, Ann Arbor staging, ECOG score, the origin of tumor cells and different therapeutic methods were analyzed.</p><p><b>RESULTS</b>According to the IPI, there were 61 cases (57.5%) with low-intermediate risk and 45 (42.5%) with intermediate-high risk. According to Ann Arbor staging, there were 8 phase I cases (7.5%), 16 phase II (15.0%), 54 phase III (51.0%) and 28 phase IV (26.5%). Twenty-five cases (23.6%) were accompanied with bone marrow invasion, 16 of them were diagnosed as lymphosarcoma cell leukemia; 38 cases with ECOG score ≥ 2; 67 cases (63.2%) had an increased LDH level; 59 cases (55.7%) had B symptom. The response rate (RR) for the whole group was 71.7%, the complete remission (CR) rate was 59.4% (63 cases), the partial remission (PR) rate was 12.3% (13 cases), the stable disease rate was 2.8% (3 cases) and the death rate was 27.4% (29 cases). The 4-year survival rate was 72.6%. Univariate analysis indicated that eight factors were related with prognosis (P < 0.05), including IPI score, Ann Arbor staging, ECOG score, the origin of tumor cells, LDH level, bone marrow invasion, different therapeutic methods and whether or not CR. Multivariate analysis showed that the origin of non-germinal center (HR = 4.24, P = 0.001), bone marrow invasion (HR = 2.08, P = 0.012), whether or not CR (HR = 2.72, P = 0.006) and therapy modality (HR = 2.58, P = 0.009) were significant factors for prognosis.</p><p><b>CONCLUSION</b>The bone marrow invasion and the origin of tumor cells are independent risk factors for prognosis. The rituximab combined with chemotherapy can significantly improve the therapeutic effect of the DLBCL, and hematopoietic stem cell transplantation is the best choice for treating patients with DLBCL.</p>


Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Young Adult , Lymphoma, Large B-Cell, Diffuse , Diagnosis , Therapeutics , Prognosis , Retrospective Studies , Risk Factors , Survival Rate , Treatment Outcome
7.
Chinese Journal of Oncology ; (12): 283-286, 2011.
Article in Chinese | WPRIM | ID: wpr-303334

ABSTRACT

<p><b>OBJECTIVE</b>To explore the risk factors for relapse after allogeneic hematopoietic stem cell transplantation (allo-HSCT) and the measures of prophylaxis and treatment.</p><p><b>METHODS</b>We summarized the clinical data of 82 patients with hematologic malignancies who were treated in our hospital from August 2003 to December 2008. Factors including age, sex, ABO blood group disparity of donor and recipient as well as the type of donor, status of disease, HLA-match, conditioning regimen, whether or not having developed acute GVHD and chronic GVHD, infusion number of CD34(+) cells, relationship between CMV infection and relapse post-transplantation were considered and analyzed.</p><p><b>RESULTS</b>Single factor analysis indicated that there were five independent risk factors related with the disease relapse (P < 0.05), including status of disease, time of diagnosis to transplantation, acute graft versus host disease (aGVHD), conditioning regimen, and chronic graft versus host disease (cGVHD). Simultaneously, the type of donor was a substantial factor (P < 0.01), determined by multi-factor Cox regression analysis. Cox regression analysis determined that disease status (OR = 2.58, 95%CI 1.26 - 5.01, P = 0.01), time from diagnosis to treatment (OR = 1.98, 95%CI 1.11 - 3.63, P = 0.025) and cGVHD (OR = 3.74, 95%CI 1.96 - 7.97, P < 0.001) were major factors for relapse of the patients who had undergone transplantation.</p><p><b>CONCLUSIONS</b>Relapse remains the primary cause of failure after allo-HSCT. Status of disease, time from diagnosis to treatment and not cGVHD are the major risk factors. Effective prevention and treatment of relapse after engraftment can improve the efficacy of HSCT.</p>


Subject(s)
Adolescent , Adult , Child , Female , Humans , Male , Middle Aged , Young Adult , Follow-Up Studies , Graft vs Host Disease , Hematologic Neoplasms , Therapeutics , Hematopoietic Stem Cell Transplantation , Infections , Recurrence , Risk Factors , Time Factors , Transplantation Conditioning , Transplantation, Homologous
8.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 401-404, 2010.
Article in Chinese | WPRIM | ID: wpr-288413

ABSTRACT

<p><b>OBJECTIVE</b>To explore the relationship between microglial proinflammatory and electromagnetic radiation and unveil the role of microglia in microwave radiation induced central nervous system injury.</p><p><b>METHODS</b>N9 microglia cells cultured in vitro were exposed to microwave at 90 mW/cm2. Cell flow cytometry was used to observe the expression of CD11b at different time points after exposure; ELISA was used to detect the concentration of TNF-alpha in N9 cell culture supernatant; RT-PCR analysis confirmed iNOS mRNA expression in N9 microglia cells; and Nitrate Reductase Method was used to test NO amount in culture supernatant.</p><p><b>RESULTS</b>The CD11b positive microglial cells increased significantly at 3 h after microwave exposure (P < 0.05), continued to increase until 24 h and peaked at 6 h after exposure. The amount of TNF-alpha rose dramatically from 1 h to 24 h after exposure (P < 0.01) and peaked at 3 h [(762.1 +/- 61.5) pg/ml] after exposure (P < 0.01). The level of NO started to increase at 1 h [(4.48-0.59) micromol/L] and lasted for 24 h after exposure. The expression of iNOS mRNA increased significantly at 1 h (P < 0.05), and tripled the original expression at 6 h after exposure, hereafter, it decreased slightly, but all were higher than the control group within 24 h after exposure.</p><p><b>CONCLUSION</b>Microwave radiation could induce the activation of microglia cells. The activated microglia cells could induce microglial proinflammatory by producing large amounts of TNF-alpha, NO, etc.</p>


Subject(s)
Animals , Mice , Cell Line , Cells, Cultured , Microglia , Metabolism , Radiation Effects , Microwaves , Nitric Oxide , Metabolism , Nitric Oxide Synthase , Metabolism , Phosphorylation , RNA, Messenger , Genetics , Tumor Necrosis Factors , Metabolism
9.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 909-913, 2010.
Article in Chinese | WPRIM | ID: wpr-293792

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effects of microwave irradiation on the expression and regulation of heat shock proteins (HSPs) in primary cultured rat hippocampal neurons.</p><p><b>METHODS</b>Neurons were exposed to 90 mW/cm(2) microwave irradiation for 10 minutes. Western blot was used to determine the expression of HSP27, HSP70, HSP90 and heat shock factor 1 (HSF1) at 0, 3, 6, 12 and 24 hour respectively. Real-time RT-PCR was used to determine the mRNA expression of HSF1. DNA-binding activity of HSF1 was measured by electrophoretic mobility shift assay (EMSA).</p><p><b>RESULTS</b>The protein expression of HSP27 was significantly increased by 22%, 36%, 18% at 3, 6, 12 h, respectively (P < 0.05). The protein expression of HSP70 was significantly increased by 23%, 32%, 26% at 3, 6, 12 h, respectively (P < 0.05, P < 0.01). The protein expression of HSP90 was significantly increased by 27%, 33% at 6, 12 h, respectively (P < 0.05, P < 0.01). The DNA-binding activity of HSF1 was stimulated, however, no significant change of the expression of HSF1 was observed on both the mRNA and protein levels.</p><p><b>CONCLUSION</b>The transcriptional activity of HSF1 is activated by microwave irradiation, which promotes the expression of HSPs. Heat shock response which contributes to establish a cytoprotective state is induced by microwave irradiation in primary cultured rat hippocampal neurons.</p>


Subject(s)
Animals , Rats , Cells, Cultured , Heat-Shock Proteins , Metabolism , Hippocampus , Metabolism , Radiation Effects , Microwaves , Neurons , Metabolism
10.
Chinese Journal of Cancer ; (12): 946-951, 2010.
Article in English | WPRIM | ID: wpr-296333

ABSTRACT

<p><b>BACKGROUND AND OBJECTIVE</b>Allogeneic hematopoietic cell transplantation (allo-HSCT) is a potent procedure for the treatment of hematologic diseases, yet it is associated with high risks of treatment-related complications. Except for transplant-related organ toxicities, renal insufficiencies which emerge earlier significantly limit patients' long survival. To analyze risk factors for acute kidney injury (AKI), we conducted a retrospective cohort study of 96 patients undergoing HSCT.</p><p><b>METHODS</b>During the first 100 days after allo-HSCT, all patients were evaluated for renal function by measuring serum creatinine clearance and glomerular filtration rate (GFR) with a classification below: Grade 0 (<25%, decline in creatinine clearance), Grade 1 (≥25% decline in creatinine clearance but <2-fold increase in serum creatinine), Grade 2 (≥2-fold rise in serum creatinine but no need for dialysis), and Grade 3 (≥2-fold rise in serum creatinine and need for dialysis). Cox regression model was used to calculate the hazard ratios (HRs) of demographic data, clinical variables, and risk factors for AKI.</p><p><b>RESULTS</b>Twenty-eight (29.2%) patients occurred Grades 1-3 renal dysfunction (Grade 1, 14 patients; Grade 2, 12 patients; Grade 3, 2 patients), and ratios of early kidney injury increased in high-risk malignancy group (HR = 2.945, 95% confidence interval (CI)=1.293-6.421), patients treated with myeloablative conditioning regimen (HR=2.463, 95% CI=1.757-4.320), and patients with acute GVHD (HR=3.553, 95% CI=1.809-6.978), sepsis (HR=3.215, 95% CI=1.189-6.333 ), or hepatic veno-occlusive disease (VOD) (HR=3.487, 95% CI=1.392-6.524). Whereas, HLA histocompatibility showed no striking increased risk for acute renal injury (HR=1.684, 95% CI=0.648-4.378). The survival rate was lower in patients with severe nephrotoxicity (21.4%) than in patients without nephrotoxicity (70.6%) (P=0.001).</p><p><b>CONCLUSIONS</b>Nephrotoxicity is the primary risk factor for AKI, severely impacting on survival. Sorts of risk factors mentioned will be useful for evaluation for kidney function of patients undergoing allo-HSCT.</p>


Subject(s)
Adolescent , Adult , Child , Female , Humans , Male , Middle Aged , Young Adult , Acute Kidney Injury , Cohort Studies , Creatinine , Blood , Graft vs Host Disease , Hematopoietic Stem Cell Transplantation , Kidney Function Tests , Leukemia, Myelogenous, Chronic, BCR-ABL Positive , General Surgery , Leukemia, Myeloid, Acute , General Surgery , Precursor Cell Lymphoblastic Leukemia-Lymphoma , General Surgery , Proportional Hazards Models , Recurrence , Retrospective Studies , Risk Factors , Survival Rate , Transplantation Conditioning , Transplantation, Homologous
11.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 553-556, 2009.
Article in Chinese | WPRIM | ID: wpr-352831

ABSTRACT

<p><b>OBJECTIVE</b>To study the change of heat shock protein (HSP)70 expression after exposure to occupational microwave in rats hippocampus, and explore the role of HSP70 in the mechanism of bio-effect of microwave irradiation.</p><p><b>METHODS</b>The animal model was established by whole body exposures in 90, 5 W/cm(2) microwave irradiation field for 20 min in rats. Changes of the mRNA of hsp70 expressions in rat hippocampus at different time were studied by RT-PCR, and the protein change by Western blot.</p><p><b>RESULTS</b>The mRNA and protein expression of hsp70 in rat hippocampus increased after 90 W/cm(2) and 5 W/cm(2) microwave irradiation for 20 min. The anal temperature and the value of SAR increased significantly. These changes were positively correlated with power and irradiation time of microwave. The results indicated that microwave irradiation led to HSP70 syntheses effectively.</p><p><b>CONCLUSION</b>Microwave irradiation can obviously induce the thermal effect and activate HSP70, and initiate the endogenous protective mechanism of central nervous system.</p>


Subject(s)
Animals , Rats , HSP70 Heat-Shock Proteins , Genetics , Metabolism , Hippocampus , Metabolism , Radiation Effects , Microwaves , RNA, Messenger , Genetics , Rats, Wistar
12.
Journal of Experimental Hematology ; (6): 713-718, 2009.
Article in Chinese | WPRIM | ID: wpr-334040

ABSTRACT

The aim of this study was to analyze the risk factors for overall survival at 5 years in 96 patients undergoing allogeneic hematopoietic stem cell transplantation by retrospective analysis. 11 clinical parameters including age, sex, disease status, HLA locus, donor type, donor-recipient blood type, conditioning regimen, aGVHD, HC, VOD and IP were selected for univariate analysis by using a Cox regression. Factors have statistic significance at the 0.1 level on univariate analysis were evaluated by multivariate analysis by a Coxs regression. The cumulative incidence of aGVHD and survival rate of patients were calculated by the method of Kaplan and Meier. The results showed that 95 patients achieved sustained donor engraftment except 1 patients. The median time of leukocyte engraftment (ANC > or = 0.5 x 10(9)/L) was 13 days. The aGVHD of I - IV grade was observed in 42 out of 96 patients (43.75%), in which 11 patients were with aGVHD of I grade (11.46%), 19 patients were with aGVHD of II grade (19.79%), 12 patients were with aGVHD of III - IV grade (12.50%). Out of 96 patients 10 relapsed and 38 dead, the overall survival at 5 years was 60.42%. The Cox regression analysis showed that aGVHD and disease status before transplant were main factors affecting long-term survival of patients, relative risks of which were 2.996 and 2.619 respectively. It is concluded that the main factors affecting long-term survival of patients are aGVHD and disease status. The key to improve the outcome of allo-HSCT is to reduce the incidence and severity of aGVHD, meanwhile to select the CR1 for allo-HSCT to treat the patients in advanced refractory and relapsed situation should be considered as important risk factors.


Subject(s)
Adolescent , Adult , Child , Female , Humans , Male , Middle Aged , Young Adult , Disease-Free Survival , Graft vs Host Disease , Mortality , Hematopoietic Stem Cell Transplantation , Mortality , Retrospective Studies , Risk Factors , Survival Rate , Transplantation, Homologous
13.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 204-207, 2007.
Article in Chinese | WPRIM | ID: wpr-357555

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the changes of cholinergic neurotrophic factors (CNTF) protein at different time points and the distribution of CNTF in rabbit retina after exposure to high power microwave (HPM), in order to determine the changes rule of CNTF protein.</p><p><b>METHODS</b>The rabbits were irradiated by HPM (peak power 90 W/cm(2)) for 15 min respectively, and then killed at 0, 3, 6, 12, 24 and 72 h after irradiation. The changes of CNTF protein were investigated by immunohistochemistry and semi-quantity analysis.</p><p><b>RESULTS</b>CNTF protein was distributed in full retinal layers, special in the cell membrane and cytoplasm. HPM irradiation could immediately down-regulated CNTF protein expression at 0 h, up-regulated and arrived at peak level at 6 h (P<0.05 vs 0 h group), and then kept control level.</p><p><b>CONCLUSION</b>HPM may cause acute retinal injure and change the expression of CNTF protein in rabbit retina. These effects show the time-dependent feature. These results suggest that CNTF activation plays a central role in the retinal injures induced by HPM, and supplies a therapy method by using foreign-aid CNTF to remedy the retinal injure induced by HPM.</p>


Subject(s)
Animals , Female , Male , Rabbits , Ciliary Neurotrophic Factor , Metabolism , Microwaves , Retina , Metabolism , Radiation Effects
14.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 215-219, 2007.
Article in Chinese | WPRIM | ID: wpr-357552

ABSTRACT

<p><b>OBJECTIVE</b>To explore the role and mechanism of glucocorticoid (GC) in the harmful bio-effects of electromagnetic irradiation.</p><p><b>METHODS</b>Rats were exposed to 65 mW/cm(2) electromagnetic wave for 20 min. At 10 min, 30 min, 3 h, 12 h after irradiation, their learning and memory abilities were tested by Morris water maze. The levels of corticosterone (CORT) in serum were measured by radioimmunoprecipitation assay and the changes of total glucocorticoid receptor (GR) expression and GR nuclear translocation in rat hippocampus were measured by reverse transcription-polymerase chain reaction and Western blot.</p><p><b>RESULTS</b>The rats had learning and memory deficits at 10 min, 30 min and 3 h after irradiation, but at 12 h had no difference from the normal control. The levels of corticosterone in serum increased significantly at 10 min, 30 min, decreased at 3 h and increased significantly compared with 12 h after irradiation. GR mRNA and total GR protein expression in rat hippocampus had no significant changes at 10 min, 30 min after irradiation. At 3 h, 12 h GR mRNA expression significantly decreased by 69%, 76% respectively and GR total protein decreased by 58%, 67% respectively. There were significant differences between the two groups and the corresponding controls (P<0.05). And compared with the control, the GR nuclear translocation increased significantly at 3 h and 12 h (P<0.05).</p><p><b>CONCLUSION</b>GC may take part in the injury to learning and memory abilities after electromagnetic irradiation, and the non-genomic and genomic effects of GC may play a major role in the early and late stage, respectively.</p>


Subject(s)
Animals , Male , Rats , Corticosterone , Blood , Electromagnetic Fields , Glucocorticoids , Blood , Hippocampus , Metabolism , Radiation Effects , Rats, Wistar , Receptors, Glucocorticoid , Metabolism
15.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 167-171, 2005.
Article in Chinese | WPRIM | ID: wpr-346544

ABSTRACT

<p><b>OBJECTIVE</b>To explore the relationship between differential activation of mitogen-activated protein kinase (MAPK) signal transduction system and apoptosis in PC12 cells induced by electromagnetic irradiation.</p><p><b>METHODS</b>Cultured PC12 cells were exposed to 65 mW/cm(2) electromagnetic wave for 20 min. The PC12 cells apoptosis was detected by flow cytometry 0, 3, 12, 24 h after electromagnetic irradiation. The phosphorylations of ERK1/2, JNK and P38 MAPK were tested by Western-blot.</p><p><b>RESULTS</b>Electromagnetic irradiation induced apoptosis in PC12 cells soon after irradiation. The apoptotic rate of PC12 cells increased to about 23.5% at 3 h. But compared with that at 3 h, there was no significant difference in the apoptotic rate at 12 h (P > 0.05). The apoptotic rate of PC12 cells increased sharply again at 24 h. After exposure to electromagnetic irradiation, the phosphorylations of ERK1/2 and JNK increased significantly. The increased phosphorylation of ERK1/2 lasted for 3 hours, but of JNK lasted for 12 hours, and 24 hours after irradiation. The phosphorylation of both ERK1/2 and JNK were significantly lower than that of control. The phosphorylation of P38 MAPK was always higher after electromagnetic irradiation, and there were two phosphorylation peaks at 3 h and 24 h.</p><p><b>CONCLUSION</b>The electromagnetic irradiation can induce the activation of MAPK signal transduction system, and ERK1/2, JNK, P38 MAPK showed differential activation. The differential activation of MAPKs may play an important role in the apoptosis of PC12 cells induced by electromagnetic irradiation.</p>


Subject(s)
Animals , Rats , Apoptosis , Radiation Effects , Blotting, Western , Flow Cytometry , MAP Kinase Kinase 4 , Metabolism , Physiology , Mitogen-Activated Protein Kinase 3 , Metabolism , Physiology , Mitogen-Activated Protein Kinases , Metabolism , Physiology , PC12 Cells , Phosphorylation , Signal Transduction , Radiation Effects , p38 Mitogen-Activated Protein Kinases , Metabolism , Physiology
16.
Chinese Journal of Applied Physiology ; (6): 10-14, 2005.
Article in Chinese | WPRIM | ID: wpr-330075

ABSTRACT

<p><b>AIM</b>To explore the effects of hypoxia on Caspases activation in cardiomyocyte and role of intracellular calcium in this event in cardiomyocytes.</p><p><b>METHODS</b>After hypoxia 0 min, 30 min, 1 h, 3 h, 6 h, 12 h, 24 h, apoptotic cell percentage was determined with Hoechst 33342 straining. Expressions of Caspases-3 mRNA and release of mitochondrial cytochrome c in primary culture of cardiomyocytes were determined by using RT-PCR and Western blotting respectively.</p><p><b>RESULTS</b>Elevation of Cyt c in cytosol was in accordance with the decline in mitochondrial Cyt c content. Significant increase in Cyt c in cytosol appeared at 12 h post hypoxia and peaked at 24 h while Cyt c in mitochondria could not be detected at 24 h post hypoxia. Hypoxia up-regulated Caspases-3 mRNA expressions beginning at 3 h post hypoxia. Intracellular calcium overload occurred earlier than release of mitochondrial Cyt c and the activation of Caspase-3 during the hypoxic insult. Inhibition of Caspase-3 activation and pretreatment with calcium chelator BAPTA/AM offered a marked protective effect on hypoxia induced cardiomyocyte apoptosis.</p><p><b>CONCLUSION</b>Hypoxia can induce mitochondrion-dependent Caspase-3 activation in cardiomyocytes and therefore leads to cell apoptosis. Increase of intracellular Ca2+ plays an important role in the activation of Caspase-3 and the induction of apoptosis in cardiomyocytes.</p>


Subject(s)
Animals , Male , Rats , Apoptosis , Calcium , Metabolism , Caspase 3 , Metabolism , Cell Hypoxia , Cytochromes c , Metabolism , Cytosol , Metabolism , Mitochondria , Metabolism , Myocytes, Cardiac , Cell Biology , Metabolism , Rats, Wistar
17.
Acta Physiologica Sinica ; (6): 89-94, 2004.
Article in Chinese | WPRIM | ID: wpr-290883

ABSTRACT

It has been demonstrated that neural cell adhesion molecule (NCAM) is critical for the induction and maintenance of long term potentiation (LTP) in the CA1 region of rat hippocampus. In the present study, we investigated the changes in NCAM mRNA expression and NCAM protein level after the induction of LTP in vitro using the techniques of in situ hybridization and Western blot. The results showed that the number of NCAM mRNA positive labelled neurons significantly increased (76.6+/-11.5 neurons) 10 min after tetanus when the slope of fEPSP markedly increased. The level of NCAM protein also increased significantly (7.190+/-0.64 arbitrary unit/50 microg protein) 10 min after tetanus. The number of NCAM mRNA positive labelled neurons no longer changed (73.3+/-14.0) 1 h after tetanus, however, the NCAM protein level (9.031+/-0.71) at 1 h after tetanus was higher than that at 10 min after tetanus. Moreover, the NMDA receptor inhibitor AP-5, which blocked LTP, prevented the increase in NCAM mRNA expression and NCAM protein level. The results demonstrate that NCAM mRNA expression maintains a high level, whereas NCAM protein changes from a low level to a high level during induction and maintenance of LTP.


Subject(s)
Animals , Male , Rats , Hippocampus , Metabolism , Physiology , Long-Term Potentiation , Physiology , Neural Cell Adhesion Molecules , Genetics , RNA, Messenger , Genetics , Rats, Wistar
18.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 104-107, 2004.
Article in Chinese | WPRIM | ID: wpr-272020

ABSTRACT

<p><b>OBJECTIVE</b>To explore molecular controlling mechanism of mitochondrial injury induced by different density of microwave irradiation.</p><p><b>METHODS</b>Rats were exposed to microwave irradiation for 1 hour at average power density of 3 mW/cm(2) or 30 mW/cm(2). After microwave irradiation, the changes of pathological ultrastructure of rat cerebral cortex and hippocampus were observed by electron microscope, and mitochondrial transcription factor A (mtTFA) mRNA expression level were determined by RT-PCR.</p><p><b>RESULTS</b>After 3 mW/cm(2) microwave irradiation for 0, 3, 24 h, mitochondrial ultrastructure and mtTFA mRNA expression level didn't significantly change in rat cerebral cortex and hippocampus. After 30 mW/cm(2) microwave irradiation for 0, 3, 24 h, mitochondrial ultrastructure obviously changed, mtTFA mRNA expression in rat hippocampus significantly increased by 67.00%, 80.00%, 30.00% respectively, and in rat cerebral cortex by 133.00%, 86.00%, 233.00% respectively. There were significant differences between the corresponding groups of hippocampus and cerebral cortex (P < 0.01).</p><p><b>CONCLUSION</b>No obvious change in mitochondria was found after 3 mW/cm(2) microwave irradiation, but it was found after 30 mW/cm(2) microwave irradiation. Mitochondria injury in cerebral cortex was more severe than that in hippocampus. mtTFA mRNA may have certain regulation in mitochondrial energy metabolism.</p>


Subject(s)
Animals , Male , Rats , Cerebral Cortex , Metabolism , Radiation Effects , DNA-Binding Proteins , Genetics , Hippocampus , Metabolism , Radiation Effects , Microscopy, Electron , Microwaves , Mitochondria , Metabolism , Radiation Effects , Mitochondrial Proteins , Genetics , Nuclear Proteins , Genetics , RNA , Genetics , Metabolism , RNA, Messenger , Genetics , Metabolism , Rats, Wistar , Reverse Transcriptase Polymerase Chain Reaction , Transcription Factors , Genetics
19.
Chinese Journal of Physical Medicine and Rehabilitation ; (12)2003.
Article in Chinese | WPRIM | ID: wpr-683284

ABSTRACT

Objective To investigate the effects of electromagnetic irradiation on activation of protein kinase C(PKC)and phosphorylation of glutamate receptor 2(GluR2)in rat cerebellum.Methods Sixty male Wistar rats were divided randomly into a control group and an electromagnetic exposure group(including 5 subgroups ob- served at different time points after the irradiation,eg.0 hour,3 hours,12 hours,24 hours and 72 hours after irradi- ation),with 10 rats in each group.All the rats in the exposure group were exposed to 90 mW/cm2 electromagnetic ir- radiation for 20 minutes,their rectal temperature was detected immediately after irradiation and the specific absorption rate(SAR)value was calculated,activation of PKC was detected with improved TaKai method,the level of cerebellar GluR2 expression and phosphorylation(ser880)was detected by using Western blot.Results Immediately(0 hour)after exposure,the rectal temperature of rats increased 2.99℃,SAR value was 8.66 W/kg.When compared to the control group,it was found that there was no significant difference between the exposure group and the control group with regard to all the parameters at 3,12,24 and 72 hours after exposure,except that the cerebellar PKC acti- vation and GluR2(ser 880)phosphorylation decreased significantly immediately after irradiation.Conclusion The electromagnetic irradiation has injurious effects on cerebellar signal pathway of for motor learning.

20.
Chinese Journal of Applied Physiology ; (6): 124-127, 2002.
Article in Chinese | WPRIM | ID: wpr-319360

ABSTRACT

<p><b>AIM</b>In order to explore the neurobiological mechanism of morphine addiction and treatment methods, the acute and chronic effects of morphine on the intracellular free calcium concentration ([Ca2+]i) in cultured hippocampal neurons were investigated.</p><p><b>METHODS</b>Changes of [Ca2+]i induced by morphine in primarily cultured hippocampal neurons were measured by confocal laser scanning microscopy using Ca(2+) -sensitive dye fluo-4 as the calcium fluorescent probe.</p><p><b>RESULTS</b>Morphine actually induced the increase in [Ca2+]i of hippocampal neurons. This process could be blocked by naltrindole (delta opioid receptor antagonist) pretreatment, but not by CTOP (micro opioid receptor antagonist) pretreatment. Pretreatment of the cells with thapsigargin almost completely blocked morphine-evoked response; while pretreatment of the cells with verapamil partially inhibited this response. After exposure to 100 micromol/L morphine for 24 h, intracellular [Ca2+]i increased and the increase could be intensified after adding 10 micromol/L naloxone to the medium.</p><p><b>CONCLUSION</b>Morphine induced the release of Ca2+ is mainly from inositol 1, 4, 5-trisphosphate (IP3) sensitive stores in hippocampal neuron of rats through activation of delta2 subtype opioid receptor.</p>


Subject(s)
Animals , Male , Rats , Calcium , Metabolism , Cells, Cultured , Hippocampus , Cell Biology , Microscopy, Confocal , Morphine , Pharmacology , Neurons , Cell Biology , Rats, Wistar
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