Changes of apoptosis, mitochondrion membrane potential and Ca2+ of hypothalamic neurons induced by high power microwave / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the injury effect and mechanism of hypothalamic neurons after high power microwave (HPM) exposure.</p><p><b>METHODS</b>Primarily cultured hypothalamic neurons were exposed to 10 and 30 mW/cm(2) HPM, and the inverted phase contrast microscope (IPCM) and flow cytometry (FCM) were employed to detect the injury of cells and change of mitochondrion membrane potential (MMP) and Ca(2+) in the cytoplasm of neurons.</p><p><b>RESULTS</b>The ratio of apoptosis was significantly higher than that of the sham exposure (P < 0.05) induced by 10 and 30 mW/cm(2) HPM and necrosis increased significantly (P < 0.05) in the group of 30 mW/cm(2) at 6 h after exposure. The content of Ca(2+) in the cytoplasm of neuron cells increased (P < 0.01) while MMP decreased significantly (P < 0.01) after radiation of 30 mW/cm(2) HPM at 6 h after exposure.</p><p><b>CONCLUSION</b>Apoptosis is one of the major death ways of hypothalamic neurons. The overloading of Ca(2+) and the decline of MMP are involved in the process.</p>

Pathological study of testicular injury induced by high power microwave radiation in rats / 中华男科学杂志

<p><b>OBJECTIVE</b>To explore the pathological characteristics and the dynamic change regularity of the testis induced by high power microwave (HPM) radiation.</p><p><b>METHODS</b>One hundred and sixty-five male Wistar rats were exposed to 0, 3, 10, 30 and 100 mW/cm2 HPM radiation for five minutes, and changes of testicular morphology and teratogenic ratio of epididymal spermatozoa were observed through light microscope and electron microscope at 6 h, 1, 3, 7, 14, 28 and 90 d after radiation.</p><p><b>RESULTS</b>Injury of testicular spermatogenic cells in rats might be induced by 3 to approximately 100 mW/cm2 HPM radiation, and the main pathological changes were degeneration, necrosis, shedding of spermatogenic cells, formation of multinuclear giant cells, decrease or loss of sperm and interstitial edema. Injury of spermatogenic cells underwent such phases as death and shedding, cavitation, regeneration and repair, characterized by being focalized, inhomogenous and phased. And the severity of pathological changes of the testis increased with power density. There was only scattered degeneration, necrosis, shedding of spermatogenic cells in the seminiferous tubule one day after 3 mW/cm2 radiation, and the pathological changes six hours after 10 mW/cm2 radiation was similar to those one day after 3 mW/cm2 radiation, but with the formation of multinuclear giant cells, and the above-mentioned pathological changes aggravated from one day to seven days after radiation. There was a significant increase in degeneration, necrosis, shedding of spermatogenic cells, as well as a significant decrease in spermatozoa and focal necrosis in simple seminiferous tubules six hours after 30 and 100 mW/cm2 radiation, and the subsequent changes were similar to those of 10 mW/cm2 radiation. There was a significant increase in teratogenic ratio of epididymal spermatozoa at 3 d, 1 to approximately 7 d, 6 h to approximately 7 d after 3, 10, 30 and 100 mW/cm2 microwave radiation respectively (P < 0.01 or P < 0.05).</p><p><b>CONCLUSION</b>HPM radiation may cause injury of testicular spermatogenic cells in rats, which has a positive correlation to radiation dosage and time.</p>

Effect of a hypothetical gene Af116609 on multi-drug resistance of gastric cancer cells / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To investigate the effect of gene Af116609 on gastric cancer multi-drug resistance (MDR) by introducing it into gastric cancer multi-drug resistant (MDR) cell line SGC7901/VCR.</p><p><b>METHODS</b>Gene Af116609 was cloned from SGC7901/VCR by RT-PCR and its differential expression between gastric cancer MDR cells and its parental cells was displayed by Northern blot. The gene was introduced to gastric cancer cells by transfection of recombinant eukaryotic expression vector by electroporation. MTT assay in vitro was applied to investigate its effect on multi-drug resistance phenotype of gastric cancer cells.</p><p><b>RESULTS</b>The full length CDS of gene Af116609, as long as 327 bp, was cloned from gastric cancer MDR cell line SGC7901/VCR and its sequence was coincident with the hypothetical gene Af116609 in GenBank. It was overexpressed in MDR cells than its parental cells at mRNA level. In the MTT assay in vitro, the drug sensitive cells transfected with sense eukaryotic expression vector showed upregulated targeted gene, with increased resistance to vincristine, 5-fliorouracil and arabinoside, and decreased resistance to adriamycin, but no influence on resistance to methotrexate. However, the drug resistant cells transfected with anti-sense eukaryotic expression vector, showed down regulated targeted gene, with less resistance to all the five anticancer drugs to different degrees.</p><p><b>CONCLUSION</b>Gene Af116609 is related to MDR phenotype of gastric cancer cells and may become a candidate molecular target to reverse the MDR of gastric cancer.</p>

Changes of the expression of beta1-adrenergic receptor and M2-muscarinic acetylcholine receptor in rat hearts after high power microwave radiation / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effect of high power microwave (HPM) radiation on the expression of beta(1)-adrenergic receptor (beta(1)-AR) and M(2)-muscarinic acetylcholine receptor (M(2)-AchR) in cardiomyocytes.</p><p><b>METHODS</b>S-band HPM device of mean power density 2 approximately 90 mW/cm(2) was used to irradiate 150 healthy Wistar male rats. Immunohistochemistry and image analysis were used to study the pathological characteristics of heart tissue and the expression of beta(1)-AR and M(2)-AchR.</p><p><b>RESULTS</b>Radiation of over 10 mW/cm(2) made myocardial fibers disordered in arrangement, degeneration even sarcoplasm condensation, Pace cells necrosis, and Purkinje cells lysis in a dose-dependent manner (r = 0.968, P < 0.05). beta(1)-AR expression in endocardium, membrane and cytoplasm of myocardium of left ventricle was increased on d1 after radiation, peaked on d3 (P < 0.05) and recovered on d14. M(2)-AchR expression was peaked on d1 (P < 0.01) and recovered on d14.</p><p><b>CONCLUSION</b>Certain degree intensity of HPM radiation may cause heart injury, and increased expressions of beta(1)-AR and M(2)-AchR, which may play an important role in the pathophysiology of heart injury induced by HPM.</p>

Studies on the injury effects of hippocampus induced by high power microwave radiation in rat / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the changes of morphology and function in rat hippocampus induced by high power microwave (HPM) radiation.</p><p><b>METHODS</b>Fifty male Wistar rats were radiated by HPM. Then their learning and memory abilities were tested with Y maze and were sacrificed 6 h, 1 d, 3 d and 7 d after radiation. The hippocampus was taken out to study the basic pathologic changes, apoptosis and the expressions of neuron-specific enolase (NSE) and glial fibrillary acidic protein (GFAP) by means of HE staining, Nissel body staining, in situ terminal end labeling and immunohistochemistry.</p><p><b>RESULTS</b>The learning and memory abilities of rats reduced significantly after HPM radiation. HPM also resulted in rarefaction, edema and hemangiectasia of hippocampus, nervous cells degeneration and necrosis, decrease or disappearance of Nissel bodies. The injuries were more serious in field CA4 and dentate gyrus, which showed dose-effect relationship, and were progressively aggravated within 7 days. The apoptosis cells were significantly increased. NSE was increased in neurons. The NSE positive areas were also seen in the interstitial matrix and blood vessels. GFAP was increased in astrocytes, which became shorter and thicker.</p><p><b>CONCLUSION</b>HPM can damage the abilities of learning and memory and results in morphologic changes in hippocampus. The major pathologic changes are degeneration, apoptosis and necrosis of neurons and edema in interstitium. NSE and GFAP play an important role in the pathologic process.</p>

Multidrug resistant effect of alternative splicing form of MAD2 gene-MAD2beta on human gastric cancer cell / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To study the effect of alternative splicing form -MAD2beta of mitotic arrest deficient protein 2 (MAD2) on the formation of multidrug resistance in human gastric adenocarcinoma cell SGC7901.</p><p><b>METHODS</b>RNA was extracted from a multidrug resistance cell line SGC7901/ADR. The full-length MAD2beta cDNA was obtained by RT-PCR and cloned into the pUCm-T vector, and then recombined into the eukaryotic expression vector pcDNA3.1 in forward direction. Subsequently, pcDNA3.1/MAD2beta vectors were then transfected into SGC7901 cells by lipofectamine. Sensitivity to drug was detected by MTT assay. Cell cycle alteration and intracellular fluorescence intensity were determined by FACS.</p><p><b>RESULTS</b>A fragment of 0.53 Kb was obtained and confirmed by DNA sequencing which was a new alternative splicing form of MAD2 named as MAD2beta. pcDNA3.1/MAD2beta transfected SGC7901 cells (SGC7901/MAD2beta) were more resistant to ADR, VCR and MMC than the control cells (SGC7901/pcDNA3.1), and also ADR fluorescence intensity of SGC7901/MAD2beta cells was lower (P < 0.05) than that of SGC7901/pcDNA3.1 cells.</p><p><b>CONCLUSION</b>MAD2beta could increase the multidrug resistance of SGC7901 cell line.</p>

The influence of high power microwave irradiation on the expression of neuropeptide Y and neural nitric oxide synthase in the rat cerebral cortex and hippocampus / 中华物理医学与康复杂志

Objective To investigate the effect of high power microwave(HPM) irradiation on neuropeptide Y (NPY) and neural nitric oxide synthase (nNOS) expression in the cerebral cortex and hippoeampus of Wistar rats. Methods A total of 110 Wistar rats were used for this study.Three groups of 30 Wistar rats were exposed to HPM irradiation at intensities of 3,10,30 and 100 mW/cm~2,respectively.Twenty rats served as controls and were ex- posed to sham HPM irradiation.At 6 h,and at 1,3,7,14 and 28 d after irradiation,five rats from each group were sacrificed,and their cerebral cortices and hippocampi were harvested.HE staining was used to highlight any change in the structure of the cerebral cortex or hippocampus.Immunohistochemistry techniques and image analysis were used to study the changes in NPY and nNOS expression.Results 10 to 100 mW/cm~2 HPM irradiation caused pyc- nosis and deep staining of some neurons in the cerebral cortex and hippocampus.The increase in nNOS expression and decrease in NPY expression observed were significant at 3 days after irradiation.Conclusion HPM irradiation can induce injury in neurons of the cerebral cortex and hippoeampus,and abnormal NPY and nNOS expression.

Effects of electromagnetic pulse on contents of amino acids in hippocampus of rats / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the relationship between the changes of amino acids contents in hippocampus of rats and electromagnetic pulse (EMP) exposure.</p><p><b>METHODS</b>Rats were decapitated and hippocampus were removed after EMP (6 x 10(4) V/m, rise time 20 ns, pulse width 30 micro s, 5 pulses in 2 minutes) irradiation, and contents of amino acids were detected with high performance liquid chromatograpy (HPLC).</p><p><b>RESULTS</b>The contents of aspartic acid (Asp) and glutamic acid (Glu) increased significantly 0, 3, 6 h after irradiation. The peak values of Asp [(17.25 +/- 1.63) pmol/ micro l] and Glu [(13.67 +/- 0.95) pmol/ micro l] were higher than those of control [(10.56 +/- 1.50), (6.94 +/- 1.10) pmol/ micro l respectively, P < 0.05]. Then both decreased gradually and reached the normal level 24 - 48 h after irradiation. The contents of glycine (Gly), taurine (Tau) and gamma-aminobutyric acid (GABA) also rose after exposure, the peak value of them [(4.51 +/- 0.60), (29.85 +/- 2.70), (5.14 +/- 0.73) pmol/ micro l respectively] were higher than those of control group [(2.18 +/- 0.31), (9.88 +/- 1.47), (2.84 +/- 0.67) pmol/ micro l, P < 0.05], then recovered 48 h after irradiation. The value of Glu/GABA increased immediately after exposure (3.45 +/- 0.25, P < 0.05), then decreased 24 h (1.62 +/- 0.23, P < 0.05) and recovered 48 h after exposure.</p><p><b>CONCLUSION</b>The toxic effect of excess excitatory amino acids may be partly responsible for the early retardation (within 24 h) of learning of rats.</p>

Relationship between expression of Bax and Bcl-2 proteins and apoptosis in radiation compound wound healing of rats / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To study the relationship between the expression of Bax, Bcl-2 proteins, and apoptosis in radiation compound wound healing of rats.</p><p><b>METHODS</b>Apoptosis, Bax and Bcl-2 proteins were estimated by in situ terminal labeling (TUNEL) and immunohistochemical methods.</p><p><b>RESULTS</b>(1) Changes of the apoptosis in wound healing showed three typical characteristics: early occurrence, high frequency and delayed disappearance after radiation to rats when compared with those of simple wound group, which might be an important reason for radiation-induced delayed wound healing. (2) The expression of Bax protein increased evidently with the increment of apoptosis and showed a good corresponding relationship with the apoptotic frequency in the process of wound healing. While the expression of Bcl-2 protein decreased obviously as the apoptosis reached a maximum and showed increasing tendency up to normal level when the apoptosis decreased distinctively.</p><p><b>CONCLUSIONS</b>Bax and Bcl-2 proteins play an important role in the apoptotic regulation of radiation compound wound healing in rats.</p>

Differential expression of RPL6/Taxreb107 in drug resistant gastric cancer cell line SGC7901/ADR and its correlation with multiple-drug resistance / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To investigate the differential expression of RPL6/Taxreb107 between drug-resistant gastric cancer cell line SGC7901/ADR and gastric cancer cell line SGC7901 as well as its correlation with multiple-drug resistance (MDR) in gastric cancer cells.</p><p><b>METHODS</b>Total RNA was extracted from SGC7901 and SGC77901/ADR, with internal control RT-PCR, Northern blot, gene cloning and expression, construction of eukaryotic expression vector, gene transfection by electroporation. The accumulation and retention of ADR in transiently transfected cell was detected by flow cytometry.</p><p><b>RESULTS</b>The internal control RT-PCR and Northern blot showed high RPL6/Taxreb107 expression in SGC7901/ADR cell line. Sense and antisense eukaryonic expression vectors demonstrated by double enzyme digestion were successfully transfected into gastric cancer cell line SGC7901 and SGC7901/ADR respectively by electroporation. The accumulation and retention of ADR detected 48 hours after transfection showed that RPL6 gene had shown effect on drug resistance in gastric cancer cell.</p><p><b>CONCLUSION</b>The high expression of RPL6/Taxreb107 in drug resistant gastric cancer cell shows its correlation with multiple-drug resistance in gastric cancer.</p>

Effect of electromagnetic pulse irradiation on structure and function of Leydig cells in mice / 中华男科学杂志

<p><b>OBJECTIVE</b>To explore the effect of electromagnetic pulse (EMP) irradiation on structure and function of Leydig cells in mice.</p><p><b>METHODS</b>One hundred and fourteen male Kunming mice were randomly divided into irradiated and control group, the former radiated generally by 8 x 10(3) V/m, 2 x 10(4) V/m and 6 x 10(4) V/m EMP respectively five times within two minutes. Pathological changes of Leydig cells were observed by light and electron microscope. Serum testosterone (T), luteinizing hormone (LH) and estradiol (E2) were measured dynamically by radioimmunoassay at 6 h, 1 d, 3 d, 7 d, 14 d and 28 d after irradiation.</p><p><b>RESULTS</b>Main pathological changes were edema and vacuolation, swelling of cytoplasmic mitochondria, reduce of lipid droplets, pale staining of most of lipid droplets, and partial or complete cavitation of lipid droplets in Leydig cells within 28 days after EMP radiation. Compared with normal controls, serum T decreased in all in different degrees within 28 days, and dropped significantly at 6 h-14 d, 6 h-7 d and 1 d-28 d after 8 x 10(3) V/m, 2 x 10(4) V/m and 6 x 10(4) V/m EMP irradiation(P < 0.05 or P < 0.01). EMP irradiation caused no significant changes in serum LH and E2.</p><p><b>CONCLUSIONS</b>Leydig cells are among those that are the most susceptible to EMP irradiation. EMP irradiation may cause significant injury in structure and function of Leydig cells in mice, whose earlier and continuous effect is bound to affect sexual function and sperm production.</p>