Behavioral Abnormality along with NMDAR-related CREB Suppression in Rat Hippocampus after Shortwave Exposure / 生物医学与环境科学（英文）

OBJECTIVE@#To estimate the detrimental effects of shortwave exposure on rat hippocampal structure and function and explore the underlying mechanisms.@*METHODS@#One hundred Wistar rats were randomly divided into four groups (25 rats per group) and exposed to 27 MHz continuous shortwave at a power density of 5, 10, or 30 mW/cm2 for 6 min once only or underwent sham exposure for the control. The spatial learning and memory, electroencephalogram (EEG), hippocampal structure and Nissl bodies were analysed. Furthermore, the expressions of N-methyl-D-aspartate receptor (NMDAR) subunits (NR1, NR2A, and NR2B), cAMP responsive element-binding protein (CREB) and phosphorylated CREB (p-CREB) in hippocampal tissue were analysed on 1, 7, and 14 days after exposure.@*RESULTS@#The rats in the 10 and 30 mW/cm2 groups had poor learning and memory, disrupted EEG oscillations, and injured hippocampal structures, including hippocampal neurons degeneration, mitochondria cavitation and blood capillaries swelling. The Nissl body content was also reduced in the exposure groups. Moreover, the hippocampal tissue in the 30 mW/cm2 group had increased expressions of NR2A and NR2B and decreased levels of CREB and p-CREB.@*CONCLUSION@#Shortwave exposure (27 MHz, with an average power density of 10 and 30 mW/cm2) impaired rats' spatial learning and memory and caused a series of dose-dependent pathophysiological changes. Moreover, NMDAR-related CREB pathway suppression might be involved in shortwave-induced structural and functional impairments in the rat hippocampus.

Microwave-induced Apoptosis and Cytotoxicity of NK Cells through ERK1/2 Signaling / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate microwave-induced morphological and functional injury of natural killer (NK) cells and uncover their mechanisms.</p><p><b>METHODS</b>NK-92 cells were exposed to 10, 30, and 50 mW/cm2 microwaves for 5 min. Ultrastructural changes, cellular apoptosis and cell cycle regulation were detected at 1 h and 24 h after exposure. Cytotoxic activity was assayed at 1 h after exposure, while perforin and NKG2D expression were detected at 1 h, 6 h, and 12 h after exposure. To clarify the mechanisms, phosphorylated ERK (p-ERK) was detected at 1 h after exposure. Moreover, microwave-induced cellular apoptosis and cell cycle regulation were analyzed after blockade of ERK signaling by using U0126.</p><p><b>RESULTS</b>Microwave-induced morphological and ultrastructural injury, dose-dependent apoptosis (P < 0.001) and cell cycle arrest (P < 0.001) were detected at 1 h after microwave exposure. Moreover, significant apoptosis was still detected at 24 h after 50 mW/cm2 microwave exposure (P < 0.01). In the 30 mW/cm2 microwave exposure model, microwaves impaired the cytotoxic activity of NK-92 cells at 1 h and down regulated perforin protein both at 1 h and 6 h after exposure (P < 0.05). Furthermore, p-ERK was down regulated at 1 h after exposure (P < 0.05), while ERK blockade significantly promoted microwave-induced apoptosis (P < 0.05) and downregulation of perforin (P < 0.01).</p><p><b>CONCLUSION</b>Microwave dose-dependently induced morphological and functional injury in NK-92 cells, possibly through ERK-mediated regulation of apoptosis and perforin expression.</p>

Real-time Assessment of Cytosolic, Mitochondrial, and Nuclear Calcium Levels Change in Rat Pheochromocytoma Cells during Pulsed Microwave Exposure Using a Genetically Encoded Calcium Indicator / 生物医学与环境科学（英文）

Little information is available about the effects of exposure to pulsed microwaves on neuronal Ca2+ signaling under non-thermal conditions. In this study, rat pheochromocytoma (PC12) cells were exposed to pulsed microwaves for 6 min at a specific absorption rate (SAR) of 4 W/kg to assess possible real-time effects. During microwave exposure, free calcium dynamics in the cytosol, mitochondria, and nucleus of cells were monitored by time-lapse microfluorimetry using a genetically encoded calcium indicator (ratiometric-pericam, ratiometric-pericam-mt, and ratiometric-pericam-nu). We established a waveguide-based real-time microwave exposure system under accurately controlled environmental and dosimetric conditions and found no significant changes in the cytosolic, mitochondrial, or nuclear calcium levels in PC12 cells. These findings suggest that no dynamic changes occurred in [Ca2+]c, [Ca2+]m, or [Ca2+]n of PC12 cells at the non-thermal level.

Heijiangdan ointment relieves oxidative stress from radiation dermatitis induced by (60)Co γ-ray in mice / 中国结合医学杂志

<p><b>OBJECTIVE</b>To investigate the effects of Heijiangdan Ointment ( HJD) on oxidative stress in (60)Co γ-ray radiation-induced dermatitis in mice.</p><p><b>METHODS</b>Female Wistar mice with grade 4 radiation dermatitis induced by (60)Co γ-rays were randomly divided into four groups (n=12 per group); the HJD-treated, recombinant human epidermal growth factor (rhEGF)-treated, Trolox-treated, and untreated groups, along with a negative control group. On the 11th and 21st days after treatment, 6 mice in each group were chosen for evaluation. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), and lactate dehydrogenase (LDH) were detected using spectrophotometric methods. The fibroblast mitochondria were observed by transmission electron microscopy (TEM). The expressions of fibroblast growth factor 2 (FGF-2) and transforming growth factor β1 (TGF-β1) were analyzed by western blot.</p><p><b>RESULTS</b>Compared with the untreated group, the levels of SOD, MDA and LDH, on the 11th and 21st days after treatment showed significant difference (P<0.05). TEM analysis indicated that fibroblast mitochondria in the untreated group exhibited swelling and the cristae appeared fractured, while in the HJD group, the swelling of mitochondria was limited and the rough endoplasmic reticulum appeared more relaxed. The expressions of FGF-2 and TGF-β1 increased in the untreated group compared with the negative control group (P<0.05). After treatment, the expression of FGF-2, rhEGF and Trolox in the HJD group were significantly increased compared with the untreated group (P<0.05), or compared with the negative control group (P<0.05). The expression of TGF-β1 showed significant difference between untreated and negative control groups (P<0.05). HJD and Trolox increased the level of TGF-β1 and the difference was marked as compared with the untreated and negative control groups (P<0.05).</p><p><b>CONCLUSION</b>HJD relieves oxidative stress-induced injury, increases the antioxidant activity, mitigates the fibroblast mitochondrial damage, up-regulates the expression of growth factor, and promotes mitochondrial repair in mice.</p>

Microwave exposure impairs synaptic plasticity in the rat hippocampus and PC12 cells through over-activation of the NMDA receptor signaling pathway / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>The aim of this study is to investigate whether microwave exposure would affect the N-methyl-D-aspartate receptor (NMDAR) signaling pathway to establish whether this plays a role in synaptic plasticity impairment.</p><p><b>METHODS</b>48 male Wistar rats were exposed to 30 mW/cm2 microwave for 10 min every other day for three times. Hippocampal structure was observed through H&E staining and transmission electron microscope. PC12 cells were exposed to 30 mW/cm2 microwave for 5 min and the synapse morphology was visualized with scanning electron microscope and atomic force microscope. The release of amino acid neurotransmitters and calcium influx were detected. The expressions of several key NMDAR signaling molecules were evaluated.</p><p><b>RESULTS</b>Microwave exposure caused injury in rat hippocampal structure and PC12 cells, especially the structure and quantity of synapses. The ratio of glutamic acid and gamma-aminobutyric acid neurotransmitters was increased and the intracellular calcium level was elevated in PC12 cells. A significant change in NMDAR subunits (NR1, NR2A, and NR2B) and related signaling molecules (Ca2+/calmodulin-dependent kinase II gamma and phosphorylated cAMP-response element binding protein) were examined.</p><p><b>CONCLUSION</b>30 mW/cm2 microwave exposure resulted in alterations of synaptic structure, amino acid neurotransmitter release and calcium influx. NMDAR signaling molecules were closely associated with impaired synaptic plasticity.</p>

Pathological changes in the sinoatrial node tissues of rats caused by pulsed microwave exposure / 生物医学与环境科学（英文）

To observe microwave induced dynamic pathological changes in the sinus nodes, wistar rats were exposed to 0, 5, 10, 50 mW/cm2 microwave. In 10 and 50 mW/cm2 groups, disorganized sinoatrial node cells, cell swelling, cytoplasmic condensation, nuclear pyknosis, and anachromasis, swollen, and empty mitochondria, and blurred and focally dissolved myofibrils could be detected from 1 to 28 d, while reduced parenchymal cells, increased collagen fibers, and extracellular matrix remodeling of interstitial cells were observed from 6 to 12 months. In conclusion, 10 and 50 mW/cm2 microwave could cause structural damages in the sinoatrial node and extracellular matrix remodeling in rats.

AduoLa Fuzhenglin down-regulates microwave-induced expression of β1-adrenergic receptor and muscarinic type 2 acetylcholine receptor in myocardial cells of rats / 生物医学与环境科学（英文）

This paper is aimed to study the effect of ADL on expression of β1-AR and M2-AchR in myocardial cells of rats exposed to microwave radiation. Immunohistochemistry, Western blot and image analysis were used to detect the expression of β1-AR and M2-AchR in myocardial cells at 7 and 14 d after microwave exposure. The results show that the expression level was higher in microwave exposure group and 0.75 g/(kg•d) ADL group than in sham operation group and significantly lower in 1.5 and 3.0 g/(kg•d) ADL groups than in microwave group. So we have a conclusion that the expression of β1-AR and M2-AchR is down-regulated in myocardial cells of rats exposed to microwave radiation. ADL can protect rats against microwave-induced heart tissue injury.

Relationship between cognition function and hippocampus structure after long-term microwave exposure / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To analyze the effects of long-term microwave exposure on hippocampal structure and function in the rat.</p><p><b>METHODS</b>Experiments were performed on 184 male Wistar rats (three exposure groups and a sham group). Microwaves were applied daily for 6 min over 1 month at average power densities of 2.5, 5, and 10 mW/cm2. Learning and memory abilities were assessed by Morris water maze. High performance liquid chromatography was used to detect neurotransmitter concentrations in the hippocampus. Hippocampal structures were observed by histopathological analysis.</p><p><b>RESULTS</b>Following long-term microwave exposure there was a significant decrease in learning and memory activity in the 7 d, 14 d, and 1 m in all three microwave exposure groups. Neurotransmitter concentrations of four amino acids (glutamate, aspartic acid, glycine, and gamma-aminobutyric acid) in hippocampus were increased in the 2.5 and 5 mW/cm2 groups and decreased in the 10 mW/cm2 group. There was evidence of neuronal degeneration and enlarged perivascular spaces in the hippocampus in the microwave exposure groups. Further, mitochondria became swollen and cristae were disordered. The rough endoplasmic reticulum exhibited sacculated distension and there was a decrease in the quantity of synaptic vesicles.</p><p><b>CONCLUSION</b>These data suggest that the hippocampus can be injured by long-term microwave exposure, which might result in impairment of cognitive function due to neurotransmitter disruption.</p>

The protective effects of Aduola Fuzhenglin on the heart injury induced by microwave exposure in rats / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the protective effects of AduoLa Fuzhenglin(ADL) on the heart injury induced by microwave exposure in rats.</p><p><b>METHODS</b>One hundred forty male Wistar rats were divided randomly into 5 groups: control, microwave radiation, 0.75 g x kg(-1) d(-1) ADL, 1.50 g x kg(-1) d(-1) ADL and 3.00 g x kg(-1) d(-1) ADL pretreatment groups. Rats in three ADL pretreatment groups were administrated by ADL per day for 2w then exposed to 30 mW/cm2 microwaves for 15 min. The left ventricle blood of rats was obtained at 7 d and 14 d after exposure to microwaves, and the blood Ca2+, AST and CK were detected with Coulter automatic biochemical analyzer, then the histological changes and ultrastructure of heart were observed under light and electron microscopes.</p><p><b>RESULTS</b>At 7 d and 14 d after exposure to microwaves, the blood Ca2+, AST and CK concentrations significantly increased (P<0.05 or P<0.01) as compared with controls; Heart muscle fibers showed wavilness, endotheliocyte karyopyknosis, anachromasis; The mitochondria swelling and cavitation, intercalary dies blurred in radiation groups. The changes in 0.75 g x kg(-1) d(-1) ADL pretreatment group were similar to the radiation group, but in 1.50 g x kg(-1)d(-1) and 3.00 g x kg(-1) d(-1) ADL pretreatment groups, above indexes of rats significantly reduced as compared with microwaves group (P<0.05); also the blood Ca2+, AST, CK contents were significantly lower than those in microwave group (P<0.05); The heart showed a tendency to improve.</p><p><b>CONCLUSION</b>Microwave radiation (30 mW/cm2) can cause the blood Ca2+, AST and CK turbulence, and heart injury in the histology and ultrastructure; ADL at the dosages of 1.50 g x kg(-1) d(-1) and 3.00 g x kg(-1) d(-1) has a protective effects on the heart injury induced by microwave in rats.</p>

Long-term microwave radiation affects male reproduction in rats / 中华男科学杂志

<p><b>OBJECTIVE</b>To investigate the effect of long-term microwave radiation on male reproduction in rats.</p><p><b>METHODS</b>A total of 100 male Wistar rats were exposed to microwave radiation with average power density of 0, 2.5, 5 and 10 mW/cm2 for 4 weeks, 5 times a week and 6 minutes per time. Changes in serum testosterone, testicular index, histology and ultrastructure, and the percentage of teratospermia in the epididymis were observed dynamically at 6 h, 7 d, 14 d, 28 d and 60 d after the exposure.</p><p><b>RESULTS</b>There was a significant decrease in serum testosterone concentration at 28 d after microwave radiation at 2.5, 5 and 10 mW/cm2 ([10.20 +/- 4.31] ng/ml, [5.56 +/- 3.47] ng/ml and [7.53 +/- 4.54] ng/ml) and at 60 d at 10 mW/cm2 ( [15.95 +/- 9.54] ng/ml), as compared with the control group ([23.35 +/- 8.06] ng/ml and [31.40 +/- 9.56] ng/ml) (P < 0.05 or P < 0.01). No significant changes were found in the testis index at 6 h -60 d after microwave radiation at the three doses, but different degrees of degeneration, necrosis and shedding of spermatogenic cells, thinning of spermatogenic epithelia, and decrease or deletion of spermatozoa were observed, and more obvious at 28 d and 60 d. Swelling and cavitation of mitochondria in all spermatogenic cells, agglutination and margin translocation of nuclear chromatin in the spermatogonial and Leydig cells were seen at 7 d and 60 d after 5 mW/cm2 microwave radiation. The rate of teratospermia of the epididymis was increased, more obviously at 7 d after 2.5, 5 mW/cm2, 60 d after 5 mW/cm2, and 7 d, 28 d and 60 d after 10 mW/cm2 microwave radiation (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>Long-term microwave radiation may cause injury to male reproduction, which is positively correlated with the radiation dose, and has an obvious late effect.</p>

Microwave radiation decreases the expressions of occludin and JAM-1 in rats / 中华男科学杂志

<p><b>OBJECTIVE</b>To explore the changes in the expressions of the tight junction related protein occludin and junctional adhesion molecule-1 (JAM-1) of the blood-testis barrier and their significance in rats after microwave radiation.</p><p><b>METHODS</b>Eighty male Wistar rats were exposed to microwave radiation with average power density of 0, 10, 30 and 100 mW/cm2 for five minutes, and dynamic changes in the expressions of testicular occludin and JAM-1 were observed by Western blot and image analysis at 6 h, 1 d, 3 d, 7 d and 14 d after the radiation.</p><p><b>RESULTS</b>There was a significant down-regulation in the expression of the occludin protein at 3 - 7 d, 6 h - 7 d and 6 h - 14 d (P < 0. 05), as well as in that of JAM-1 at 3 - 7 d, 1 - 7 d and 1-14 d (P < 0.05) after exposure to 10, 30 and 100 mW/cm2 microwave radiation.</p><p><b>CONCLUSION</b>The decreased protein expressions of occludin and JAM-1 may play an important role in the microwave radiation induced-damage to the blood-testis barrier.</p>

Effects of electromagnetic radiation on RAF/MEK/ERK signaling pathway in rats hippocampus / 中国应用生理学杂志

<p><b>AIM</b>To study the development of changes for signaling molecules related to Raf/MEK/ERK pathway in hippocampus of rats after electromagnetic radiation, and investigate the mechanisms of radiation injury.</p><p><b>METHODS</b>Rats were exposed to X-HPM, S-HPM and EMP radiation source respectively, and animal model of electromagnetic radiation was established. Western blot was used to detect the expression of Raf-1, phosphorylated Raf-1 and phospholylated ERK.</p><p><b>RESULTS</b>The expression of Raf-1 down-regulated during 6 h-14 d after radiation, most significantly at 7 d, and recovered at 28 d. There was no significant difference between the radiation groups. The expression of phosphorylated Raf-1 and phosphorylated ERK both up-regulated at 6 h and 7 d after radiation, more significantly at 6 h, and the two microwave groups were more serious for phosphorylated ERK. During 6 h-14 d after S-HPM radiation, the expression of phosphorylated Raf-1 increased continuously, but phosphorylated ERK changed wavily, 6 h and 7 d were expression peak.</p><p><b>CONCLUSION</b>Raf/MEK/ERK signaling pathway participates in the hippocampus injury induced by electromagnetic radiation. The excessive activation of ERK pathway may result in the apoptosis and death of neurons, which is the important mechanism of recognition disfunction caused by electromagnetic radiation.</p>

Effect of microwave radiation on primary cultured Sertoli cells / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore whether microwave radiation may cause injury of primary cultured Sertoli cells.</p><p><b>METHODS</b>The model of primary cultured Sertoli cells in vitro was established, which was radiated by microwave with average power density 0, 30 and 100 mW/cm(2) for five minutes. The changes of cell cycle, apoptosis and death, and intracellular Ca2+ concentration in the Sertoli cells were measured at sixth hours through Annexin V-PI double labeling and Fluo-3-AM labeling, flow cytometry combined with laser scanning confocal microscopy after microwave exposure.</p><p><b>RESULTS</b>The numbers of Sertoli cells were obviously reduced in G0-G1 and G2-M phase (62.57% +/- 3.22% and 8.25% +/- 1.75%) and increased in S phase (29.17% +/- 4.87%) compared with the control groups (79.18% +/- 0.24%, 11.17% +/- 0.50% and 9.64% +/- 0.62%) (P < 0.05 or P < 0.01), but the changes of rate of apoptosis and death and intracellular Ca2+ concentration showed no difference at 6 h after exposure to 30 mW/cm(2) microwave. There was a significant increase in the Sertoli cell counts of G0-G1 phase (87.69% +/- 1.32%), and decrease in the Sertoli cell counts of G2-M and S phase (7.41% +/- 0.60% and 4.87% +/- 0.91%) (P < 0.01). There was also a significant increase in intracellular Ca2+ concentration and rate of apoptosis and death (P < 0.05 or P < 0.01) at 6 h after exposure to 100 mW/cm(2) microwave.</p><p><b>CONCLUSION</b>100 mW/cm(2) microwave radiation may cause growth inhibition and increase of apoptosis and death in the primary cultured Sertoli cells. The increase of intracellular Ca2+ concentration is one of the injury mechanisms.</p>

A aquaporin 4 expression and effects in rat hippocampus after microwave radiation / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the expression of aquaporin 4 (AQP4) after microwave exposure and the correlation with the brain injury by radiation.</p><p><b>METHODS</b>70 male rats were exposed to microwave whose average power density was 0, 10, 30 and 100 mW/cm(2) respectively. Rats were sacrificed at 6 h, 1 d, 3 d and 7 d after exposure. Immunohistochemistry and Western blot were used to detect the expression of AQP4 in protein level in rat hippocampus, and the expression of AQP4 in gene level was measured by in situ hybridization and RT-PCR.</p><p><b>RESULTS</b>The expression of AQP4 in rat hippocampus was abnormal after 10, 30, 100 mW/cm(2) microwave exposure. The protein level showed increased at first and then recovered at 10 and 30 mW/cm(2) groups, while increased progressively in 100 mW/cm(2) group within 14 d (P < 0.01). The gene expression of AQP4 was increased (0.51 +/- 0.02) at the beginning (6 h) and then regained after 10 mW/cm(2) microwave exposure, while in 30 and 100 mW/cm(2) groups, it rose to the peak at 7 d (0.46 +/- 0.02 and 0.43 +/- 0.08) and didn't get back (P = 0.004; P = 0.012).</p><p><b>CONCLUSION</b>Microwave radiation can increase the expression of AQP4 in rat hippocampus. The change might participate in the process of increasing permeability of blood-brain barrier and lead to the brain edema after microwave radiation.</p>

Influence of electromagnetic radiation on raf kinase inhibitor protein and its related proteins of hippocampus / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the development of changes for Raf kinase inhibitor protein (RKIP) and its mRNA in rats hippocampus after electromagnetic radiation.</p><p><b>METHODS</b>Rats were exposed to X-band high power microwave (X-HPM), S-band high power microwave (S-HPM) and electromagnetic pulse (EMP) radiation source respectively. The animal model of electromagnetic radiation was established. Western blot was used to detect the expression of RKIP, and RT-PCR was applied to detect the expression of RKIP mRNA. The interaction of RKIP and Raf-1 was measured with co-immunoprecipitation method, and the expression of cerebral choline acetyltransferase (CHAT) was measured by immunohistochemistry.</p><p><b>RESULTS</b>The expression of RKIP significantly down-regulated at 6 h after radiation, and recovered at 1 d in group EMP, but the down-regulation continued during 1 approximately 7 d after radiation in the two microwave groups. The expression of RKIP mRNA changed wavily during 6 h approximately 7 d after radiation, which showed down-regulation at 6 h, and up-regulation at 3 d. The interaction of RKIP and Raf-1 decreased during 6 h approximately 7 d after radiation, most significantly at 7 d, and the two microwave groups were more significant. The expression of CHAT decreased continuously during 6 h approximately 7 d after radiation, and generally recovered on 14 d.</p><p><b>CONCLUSION</b>The down-regulation of RKIP and its related proteins of hippocampus is induced by electromagnetic radiation.</p>

High power microwave radiation damages blood-testis barrier in rats / 中华男科学杂志

<p><b>OBJECTIVE</b>To determine the effect of high power microwave (HPM) radiation on the structure and function of blood-testis barrier (BTB) in rats.</p><p><b>METHODS</b>One hundred and sixty-six male Wistar rats were treated by heart perfusion of lanthanum-glutaraldehyde solution and tail vein injection of evans blue (EB) at 6 h, 1, 3, 7 and 14 d after exposed to 0, 10, 30 and 100 mW/cm2 HPM radiation for 5 minutes, the structural change of BTB and distribution of lanthanum or EB observed through the light microscope, electron microscope and laser scanning confocal microscopy (LSCM).</p><p><b>RESULTS</b>Testicular interstitial edema, vascular congestion or hyperemia with accumulation of plasma proteins and red blood cells in the inner compartment of seminiferous tubules were observed after exposure to HPM. The above-mentioned pathological changes were aggravated at 1-7 d and relieved at 14 d after radiation, obviously more severe in the 30 and 100 mW/cm2 exposure groups than in the 10 mW/cm2. Both lanthanum precipitation and EB were deposited in the inner compartment.</p><p><b>CONCLUSION</b>HPM radiation may damage the structure and increase the permeability of BTB.</p>

Influence of microwave radiation on synaptic structure and function of hippocampus in Wistar rats / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effect of microwave radiation on synaptic structure, characteristic of synaptosome, the contents and release of neurotransmitters in hippocampus in Wistar rats.</p><p><b>METHODS</b>Wistar rats were exposed to microwave radiation with average power density of 30 mW/cm(2). Electron telescope was used to study the change of the synaptic structure at 6 h after radiation and to identify synaptosome. Flow cytometry and electron spin resonance were used to study the change of the concentration of Ca(2+) in synapse and the fluidity of membrane proteins of synaptosome. High performance liquid chromatography (HPLC) and spectrophotometer were used to study the changes of contents and release of amino acids and acetylcholine in hippocampus.</p><p><b>RESULTS</b>Microwave radiation of 30 mW/cm(2) caused deposits of synapse vesicle, elongation of active zone, the increase of thickness of postsynaptic density (PSD) and curvature, and perforation of synapse. The concentration of Ca(2+) in synapse (P<0.01) and tc of membrane proteins (P<0.01) of synaptosome increased contents of glutamic acid and glycine (P<0.01) and release of GABA increased the increase of contents and release of acetylcholine, and activity of acetyl cholinesterase (P<0.01) increased.</p><p><b>CONCLUSION</b>Microwave radiation can induce the injure of synaptic structure and function of hippocampus, and then induce the disorder of the ability of learning and memory in rats.</p>

Effect of Xuebijing injection(血必净注射液) combined with dexamethasone in prevention and treatment of chronic pulmonary injury Induced by paraquat in rats / 中国中西医结合急救杂志

Objective To explore the possible mechanism and protective effect of Xuebijing injection (血必净注射液)and dexamethasone on rats with paraquat-induced chronic pulmonary injury.Methods Thirty male Wistar rats were randomly divided into six groups:normal group(n=5),model group(n=5), treatment groups(n=20).In the normal group,normal saline was used,while in the other groups,20% paraquat 80 mg/kg was injected peritoneally for poisoning.After 2 hours of intoxication,low dose Xuebijing injection(1.25 g/kg),high dose Xuebijing injection(2.50 g/kg),dexamethasone(25 mg/kg),high dose Xuebijing injection combined with dexamethasone(combined group)respectively were administered into the four different treatment groups,equal amount of normal saline was given to the normal and model groups,and the treatment continued for 4 days.At 28 days after paraquat injection,5 rats in each group were killed respectively,serum transforming growth factor-?1(TGF-?1)and hydroxyproline(HYP)level in the lung homogenate were measured,and pulmonary coefficient and histological changes were observed.Results In the treatment groups,the levels of serum TGF-?1 and lung tissue HYP,pulmonary coefficient were leas than those of model group,and among the treatment groups,combined group had the best results(all P

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>