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To estimate the detrimental effects of shortwave exposure on rat hippocampal structure and function and explore the underlying mechanisms.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.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.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.

Objective To investigate the effects of Heijiangdan Ointment (黑绛丹膏, HJD) on oxidative stress in 60Co γ-ray radiation-induced dermatitis in mice.

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.

Background: To investigate the renal pathophysiologyin rhabdomyolysis-induced acute kidney injury (AKI) in rats under hypoxia and deprivation of food and water (HDFW), thus broadening the knowledge about rhabdomyolysis-induced AKI in massive earthquake. Methods: Male Wistar rats weighing 200-230g were randomized into control, rhabdomyolysis (R), HDFW and rhabdomyolysis in combination with HDFW (R/HDFW) group. Experimental rhabdomyolysis rat model was established through clamping hind limb muscles, HDFW model rats were kept in 10% hypoxic chamber unavailable to food and water. At 1, 3, 5, 7, 9, 11d after treatment, serum creatinine (Scr) level, renal index, renal structural changes and cell apoptosis were analyzed. Results: After R, HDFW, R/HDFW treatment, the animals showed significantly higher Scr levels than the control group. Renal index in R and R/HDFW groups elevated remarkably compared with that in control and HDFW group. The results of histopathology, ultra-structure and apoptosis assay suggested that rhabdomyolysis caused renal tubular injury, HDFW treatment resulted in renal vascular dilation, tissue congestion and tubular cell damage. In addition, more severe renal lesion appeared in R/HDFW. Conclusions: We conclude that the association of experimental rhabdomyolysis with HDFW results in a different functional and histological pattern. The rhabdomyolysis-HDFW combination causes more severe renal injury.

To identify gene expression changes and the role of activating transcription factor 3 (ATF3) in hemin toxicity in renal tubular epithelial cells, then elucidate molecular mechanisms of hemin toxicity on renal tubular epithelial cells.An oligo array comprising 35,035 genes was used to compare differential gene expression in hemin-treated and non-treated HK-2 cells (human renal proximal tubular epithelial cells), and the role of ATF3 in hemin toxicity was assessed using siRNA technique.A total of 128 mRNAs were at least twofold up-regulated and 101 mRNAs were at least twofold down-regulated after hemin treatment. Expression levels of ATF3, heat shock protein 70, c-fos, and c-jun were remarkably increased. Hemin also suppressed nuclear factor-kappa B inhibitor α, β-2 adrenergic receptor, and interleukin-6 mRNA amounts more than twofold. We further demonstrated the protective role of ATF3 in hemin cytotoxicity.The data suggest that hemin caused multiple changes of gene expression in HK-2 cells, and ATF3 protects against hemin cytotoxicity.

To investigate microwave-induced morphological and functional injury of natural killer (NK) cells and uncover their mechanisms.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.Microwave-induced morphological and ultrastructural injury, dose-dependent apoptosis (P0.001) and cell cycle arrest (P0.001) were detected at 1 h after microwave exposure. Moreover, significant apoptosis was still detected at 24 h after 50 mW/cm2 microwave exposure (P0.01). 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 (P0.05). Furthermore, p-ERK was down regulated at 1 h after exposure (P0.05), while ERK blockade significantly promoted microwave-induced apoptosis (P0.05) and downregulation of perforin (P0.01).Microwave dose-dependently induced morphological and functional injury in NK-92 cells, possibly through ERK-mediated regulation of apoptosis and perforin expression.

There has been growing public concern regarding exposure to microwave fields as a potential human health hazard. This study aimed to identify sensitive biochemical indexes for the detection of injury induced by microwave exposure. Male Wistar rats were exposed to microwaves for 6 min per day, 5 days per week over a period of 1 month at an average power density of 5 mW/cm(2) (specific absorption rate of 2.1 W/kg). Urine specimens were collected over 24 h in metabolic cages at 7 days, 21 days, 2 months, and 6 months after exposure. (1)H NMR spectroscopy data were analyzed using multivariate statistical techniques. Urine metabolic profiles of rats after long-term microwave exposure were significantly differentiated from those of sham-treated controls using principal component analysis or partial least squares discriminant analysis. Significant differences in low molecular weight metabolites (acetate, succinate, citrate, ketoglutarate, glucose, taurine, phenylalanine, tyrosine, and hippurate) were identified in the 5 mW/cm(2) microwave exposure group compared with the sham-treated controls at 7 days, 21 days, and 2 months. Metabolites returned to normal levels by 6 months after exposure. These data indicated that these metabolites were related to the perturbations of energy metabolism particularly in the tricarboxylic acid cycle, and the metabolism of amino acids, monoamines, and choline in urine represent potential indexes for the detection of injury induced by long-term microwave exposure.

Objective To investigate the effects and ascertain the significance of microwave radiation on the expression of phosphorylated cyclic adenosine monophosphate (cAMP)-response element-binding protein (pCREB), cAMP-responsive element modulator (CREM), and CREB-binding protein (CBP) in the testicular tissue of rats. Methods Thirty male Wistar rats were randomly divided into control group (n=5) and radiation group (n=25). Five rats in the radiation group were sacrificed at 6h, 1, 3, 7, and 14d, respectively, after exposure to microwave radiation for 5min, with an average power density of 30mW/cm2. Rats in the control group were sacrificed within 1d without receiving microwave radiation. Expressions and dynamic changes in pCREB, CREM, and CBP in the testicular tissues were examined by immunohistochemistry and Western blotting. Results pCREB, CREM, and CBP were mainly expressed in the sperm nuclei of the seminiferous tubule in the rat testis. pCREB and CBP protein expressions were downregulated from 6h to14d (except for pCREB at 1d) after exposure to microwave radiation (P < 0.05 or P < 0.01). The expression of CREM was also weakened significantly from 6h to 7d after radiation (P < 0.05 or P < 0.01). Conclusion The downregulation of pCREB, CREM, and CBP expression may play an important role in the injury of spermatogenic cells caused by microwave radiation.

Change of HIF-1α/ERK signaling pathway and its significance in the damage of the hippocampus induced by microwave exposure provides new targets for in-depth study of microwave injury mechanisms and prevention and control measures and approaches. 100 male Wistar rats were exposed to microwave at 2.5, 5 and 10 mW/cm2. The exposure time was 6 min/times, 5 times/week, and the exposure was continuous for one month. Rats were sacrificed at 6 h, 7 d, 14 d, one and two months after exposure. The expression of hif-1α mRNA in hippocampus was detected by real-time PCR. HIF-1α, ERK1/2, p-ERK1/2 expression were detected by Western blot, IHC and image analysis. The mRNA and protein levels of HIF-1α in hippocampus were increased significantly at 14 d and one month in 2.5 and 5 mW/cm2 groups, while decreased from 14 d to two months in 10 mW/cm2 group. There was no significant change of ERK1/2 within two months in exposure groups. In sham group, p-ERK1/2 was expressed weakly positive in neuron cytoplasm of hippocampus, while there was no changes in 2.5 mW/cm2 group, and p-ERK1/2 was expressed positive or strong positive from 7 d to one month in 5 and 10 mW/cm2 group. Therefore, HIF-1α and p-ERK1/2 expression in hippocampus were changed after 2.5, 5 and 10 mW/cm2 microwave exposure, which indicated the activation of HIF-1α and ERK pathway participated in the processes of hippocampus mitochondria injury induced by microwave, and might repair the mitochondria injury.

Objective To observe the changes in occludin expression in hippocampus of rats injured by long-term microwave exposure at low dosage,and explore the mechanism of the effect of occludin on microwave-induced blood-brain barrier(BBB) injury.Methods A total of 156 male Wistar rats were assigned into 4 groups(39 each) according to the microwave dosage they received(0,2.5,5 and 10 mW/cm2).Irradiation was given 5 times/week and 6 minutes for each exposure for one month.Five rats of each group were sacrificed at each time point(6h and day 7,14,30 and 60 after irradiation),the structural changes in hippocampus tissues BBB were observed by light and electron microscopy.Another 3 rats of each group were sacrificed after an intravenous injection of 2% Evans blue(EB) at the time points of 6h and day 7 and 30 after irradiation,and the change in BBB permeability was examined by laser scanning confocal microscopy.Western blotting,real-time PCR and image analysis were used to detect the gene and protein expression of occludin in hippocampus of rats.Results After microwave irradiation in doses of 2.5,5 and 10 mW/cm2,respectively,on day 7,14 and 30,the astrocytes were found to be swollen,the capillary gaps of hippocampus were broadened and tight junction(TJ) structure was inconspicuous or widened.In sham-group(0 mW/cm2),the red fluorescence of EB was limited in lumens of blood vessels,while in 5 and 10 mW/cm2 groups,Evans blue was dispersed surrounding the blood vessels at 6h and day 7 till day 30 in an irradiation dose-dependent manner.In 5 and 10 mW/cm2 groups,the expression of occludin protein in hippocampus decreased at day 14(P < 0.05) and day 7(P < 0.01),and a remarkable decrease appeared at day 30 in both groups(P < 0.01),followed by a recovery to the sham-group level at day 60(P > 0.05).In the 2.5,5 and 10 mW/cm2 groups,mRNA expression of occludin began to significantly decrease at day 7 and 14 and it lowered to the nadir at day 30(P < 0.01),followed by a recovery to the level of the sham-group at day 60(P > 0.05).Conclusions A long-term microwave irradiation with dosage of 2.5 to 10 mW/cm2 may destroy the structure of BBB of rats’ hippocampus and increase permeability in a radiation-dose-dependent manner.The results suggest that the decrease of occludin expression may play a part in the changes in BBB permeability induced by microwave irradiation.

Objective To explore the effects of microwave radiation on the morphology and function of hematopoietic system in rats.Methods One hundred and forty-four male Wistar rats randomly divided into 4 groups(36 each) were exposed to microwave radiation at the average power density of 0,2.5,5 and 10 mW/cm2 respectively(0 mW/cm2 as sham group),with one exposure of 6 minutes,5 times per week,up to a total of 30 days.Six rats of each group were respectively sacrificed at 6 hours and 7,14,30,60 and 180 days post radiation to obtain blood samples in the inferior vena cava for counting leukocytes,erythrocytes and platelets,and detecting the concentration of hemoglobin.Additionally,bone marrow in sternum was obtained from sacrificed rats of each group for evaluation of histological and ultrastructural changes by light and electron microscopy.Results Compared with the sham group,a reduction,in different degree,was seen in numbers of white cells,neutrophils and erythrocytes 6 hours after radiation in 5mW/cm2 group,while a raise was seen in numbers of erythrocytes and platelets 60 days after radiation.At 180 days post radiation,a significant decrease was seen in total number of leukocytes and numbers of lymphocytes and platelets in 5mW/cm2 and 10mW/cm2 groups when compared with the sham group.Under light microscope,no dramatic changes was seen in the hematopoiesis cells of bone marrow at day 14 post radiation,obvious hyperemia and edema of interstitial tissue were seen at day 30 post radiation,while a reduction in hematopoiesis cells and an increase in adipocytes,both in a dose dependent manner,were seen at day 180.At day 7 post radiation,apoptosis and necrosis was seen in trilineage hematopoietic cells of bone marrow of 5mW/cm2 group under electron microscope.Conclusion A Long-term exposure to the microwave,ranging from 5 to 10mW/cm2,will result in morphological and functional changes,in a dose-dependant manner,in the hematopoietic system of rats.

Human hepassocin (HPS) was originally detected by subtractive and differential cDNA cloning as a liver-specific gene that was markedly upregulated during liver regeneration. Previous studies suggested that HPS showed mitogenic activity on isolated hepatocytes in vitro. However, its in vivo functions remained largely unknown. Therefore, the function of recombinant human HPS during liver regeneration and chemically induced liver injury was investigated.The proliferation of primary hepatocytes was examined by [(3)H]thymidine incorporation and immunohistological staining of proliferating cell nuclear antigen (PCNA). RNA interference was performed to knock down the endogenous expression of HPS. The proliferation of L02 cells was examined by MTS assay. The phosphorylation of ERK1/2 (extracellular signal-regulated kinase 1/2) was investigated by western blotting analysis. Assessment of liver injury (histology, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels) and of apoptosis, by TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling) assay, was performed.Purified recombinant human HPS showed specific mitogenic activity on primary hepatocytes and normal liver cell lines in a mitogen-activated protein kinase (MAPK)-dependent manner and stimulated the proliferation of hepatocytes in rats with 70% partial hepatectomy. Administration of HPS to rats after d-galactose and carbon tetrachloride (CCl(4)) treatment protected against liver injury (minimal liver necrosis, depressed ALT and AST levels, and decreased lethality), reduced apoptosis and enhanced proliferation. Knock-down of endogenous HPS in vivo enhanced the liver injury induced by d-galactose by increasing the apoptosis and elevating ALT and AST levels.HPS is a hepatic growth factor which can accelerate hepatocyte proliferation in vivo and protect against liver injury. These data point to the potential interest of HPS in the treatment of fulminant hepatic failure.

Studies were performed to determine the effects of microwave on synaptic vesicles and the expression of synaptic vesicular associated proteins including synapsin I, VAMP-2, syntaxin, and synaptophysin. 25 Wistar rats were exposed to microwave which the average power density was 30 mW/cm2, and whole body average specific absorption rate was 14.1 W/kg for 5 min. Synaptosome preparations in the cerebral cortex and hippocampus were obtained by isotonic Percoll/sucrose discontinuous gradients at 6 h, 1, 3, and 7 days after radiation. The expression of synaptic vesicular associated proteins was measured using Western blots and image analysis. The interaction between VAMP-2 and syntaxin was examined by coimmunoprecipitation analysis. Synapsin I in the cerebral cortex were decreased at 3 days (P < 0.01) after radiation and in the hippocampus increased at 1 day (P < 0.01), decreased at 3 days (P < 0.01), increased again at 7 days (P < 0.01) after exposure, compared with the sham-treated controls. Synaptophysin were increased in 1–7 days (P < 0.01) after exposure in the cerebral cortex and hippocampus. VAMP-2 were decreased at 1 and 3 days (P < 0.01) and syntaxin were decreased in 6 h to 3 days (P < 0.01) after radiation in the cerebral cortex and hippocampus. The interactions between VAMP-2 and syntaxin were decreased at 3–7 days (P < 0.01) after radiation in the cerebral cortex and hippocampus, compared with the sham-treated controls. These results suggest that 30 mW/cm2 (SAR 14.1 W/kg) microwave radiation can result in the perturbation of the synaptic vesicles associated proteins: synapsin I, synaptophysin, VAMP-2, and syntaxin. The perturbation could induce the deposit of synaptic vesicle, which might be relative to the dysfunction of the synaptic transmission, even the cognition deficit. Synapse 63:1010–1016, 2009. © 2009 Wiley-Liss, Inc.

To investigate the mechanisms of microwave induced pacemaker cell injuries, Wistar rats and the primary pacemaker cells of newborn Wistar rats were exposed to microwave at average power density of 50 mW/cm 2 . Slower spontaneous beating rate, intercellular Ca 2+ aggregation and cell membrane perforation were detected immediately after the exposure. Moreover, hyperpolarization-activated cyclic nucleotide-gated cation channel 4 (HCN4) was down-regulated immediately after the exposure and up-regulated at 12 h after the exposure. In the sinoatrial node (SAN) of the rats, HCN4 expression increased from day 1 to day 28 after microwave exposure, then declined from 3rd month to 6th month, which was consistent with the changes of ratio of β1-adrenergic receptor (β1-AR) and muscarinic type 2 acetylcholine receptor (M2-AchR). In conclusion, dynamic expression of HCN4, together with changes of β1-AR and M2-AchR expression, was involved in microwave induced pacemaker cell injuries.

The purpose of this paper is to explore the change of NF-κB signaling pathway in intestinal epithelial cell induced by fission neutron irradiation and the influence of the PI3K/Akt pathway inhibitor LY294002. Three groups of IEC-6 cell lines were given: control group, neutron irradiation of 4Gy group, and neutron irradiation of 4Gy with LY294002 treatment group. Except the control group, the other groups were irradiated by neutron of 4Gy. LY294002 was given before 24 hours of neutron irradiation. At 6 h and 24 h after neutron irradiation, the morphologic changes, proliferation ability, apoptosis, and necrosis rates of the IEC-6 cell lines were assayed and the changes of NF-κB and PI3K/Akt pathway were detected. At 6 h and 24 h after neutron irradiation of 4Gy, the proliferation ability of the IEC-6 cells decreased and lots of apoptotic and necrotic cells were found. The injuries in LY294002 treatment and neutron irradiation group were more serious than those in control and neutron irradiation groups. The results suggest that IEC-6 cells were obviously damaged and induced serious apoptosis and necrosis by neutron irradiation of 4Gy; the NF-κB signaling pathway in IEC-6 was activated by neutron irradiation which could protect IEC-6 against injury by neutron irradiation; LY294002 could inhibit the activity of IEC-6 cells.

Recent studies have highlighted the important role of the postsynaptic NMDAR-PSD95-CaMKII pathway for synaptic transmission and related neuronal injury. Here, we tested changes in the components of this pathway upon microwave-induced neuronal structure and function impairments. Ultrastructural and functional changes were induced in hippocampal neurons of rats and in PC12 cells exposed to microwave radiation. We detected abnormal protein and mRNA expression, as well as posttranslational modifications in the NMDAR-PSD95-CaMKII pathway and its associated components, such as synapsin I, following microwave radiation exposure of rats and PC12 cells. Thus, microwave radiation may induce neuronal injury via changes in the molecular organization of postsynaptic density and modulation of the biochemical cascade that potentiates synaptic transmission.

To investigate the effects of Heijiangdan Ointment ( HJD) on oxidative stress in (60)Co γ-ray radiation-induced dermatitis in mice.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.Compared with the untreated group, the levels of SOD, MDA and LDH, on the 11th and 21st days after treatment showed significant difference (P0.05). 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 (P0.05). After treatment, the expression of FGF-2, rhEGF and Trolox in the HJD group were significantly increased compared with the untreated group (P0.05), or compared with the negative control group (P0.05). The expression of TGF-β1 showed significant difference between untreated and negative control groups (P0.05). HJD and Trolox increased the level of TGF-β1 and the difference was marked as compared with the untreated and negative control groups (P0.05).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.

Objective: The incidence of carcinoma of extrahepatic bile duct tends to increase during recent decade in China, but its cause is unclear. This study is to investigate the Hepatitis C virus (HCV) and Hepatitis B virus (HBV) infection in the tissues of carcinoma of extrahepatic bile duct and study their correlation. Methods: HCV RNA and HBV DNA was detected byin situ polymerase chain reaction (IS-PCR) in sections of 51 cases of carcinoma of extrahepatic bile duct and 34 cases of control group. Results: Of 51 carcinoma of extrahepatic bile duct, HCV RNA was detected in 18 (35.4%), HBV DNA in 8 (15.9%). In 34 cases of control group, HCV RNA was detected in 2 (5.9%), and HBV DNA in 3 (8.8%). Conclusion: The prevalence of hepatitis C and B viral infection in the tissues of carcinoma of extrahepatic bile duct was significantly higher than in control group. The findings suggest a correlation between HCV, HBV infection and carcinoma of extrahepatic bile duct, inferring HCV and HBV might be involved in the development of carcinoma of extrahepatic bile duct.

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.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 HE 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.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.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.

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.

Neutron irradiation (IR) has been proven to cause more serious damage than gamma IR. Preventing and curing neutron IR damage remains an urgent issue. The objective of this study was to investigate the radioprotective effects of IL-11 against neutron IR-induced damage in small intestine of mice. Mice were exposed to 3-Gy neutron IR whole body and then treated with 500 μg/kg interleukin-11 (IL-11) intraperitoneally every day. Mice were observed at various time-points over 1–5 days after IR. IEC-6 cells were exposed to 4 Gy neutron IR, and 100 ng/mL rhIL-11 was added to culture medium. Cell proliferation activity was estimated by MTT assay and rates of apoptosis were estimated by flow cytometry. IL-11 slightly alleviated the incidence of diarrhea in the mice and promoted intestinal epithelia regeneration. In the in vitro study, neutron IR activated extracellular signal-regulated kinase (ERK)1/2 phosphorylation in intestinal epithelial cells constitutively, which was initially suppressed and then activated later by IL-11. The MEK-specific inhibitor U0126 could antagonize the positive effect of IL-11 on cell growth. Phosphatidylinositol 3-kinase (PI3K)/Akt pathway activation was suppressed after neutron IR, but could be triggered by IL-11 to protect the cells. The PI3K inhibitor LY294002 suppressed the positive effect of IL-11 on cell growth, and antagonized the protective effect of IL-11 against cell death after neutron IR. IL-11 increases cell proliferation after neutron IR in MEK and PI3K-dependent signaling pathways, but protects cells against death only in the PI3K-dependent signaling pathway.

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.

To study the protective effects of AduoLa Fuzhenglin(ADL) on the heart injury induced by microwave exposure in rats.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.At 7 d and 14 d after exposure to microwaves, the blood Ca2+, AST and CK concentrations significantly increased (P0.05 or P0.01) 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 (P0.05); also the blood Ca2+, AST, CK contents were significantly lower than those in microwave group (P0.05); The heart showed a tendency to improve.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.

To analyze the effects of long-term microwave exposure on hippocampal structure and function in the rat.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.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.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.

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.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.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.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.

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.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.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 (P0. 05), as well as in that of JAM-1 at 3 - 7 d, 1 - 7 d and 1-14 d (P0.05) after exposure to 10, 30 and 100 mW/cm2 microwave radiation.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.

To explore whether microwave radiation may cause injury of primary cultured Sertoli cells.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.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%) (P0.05 or P0.01), 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%) (P0.01). There was also a significant increase in intracellular Ca2+ concentration and rate of apoptosis and death (P0.05 or P0.01) at 6 h after exposure to 100 mW/cm(2) microwave.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.

To investigate the expression of aquaporin 4 (AQP4) after microwave exposure and the correlation with the brain injury by radiation.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.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 (P0.01). 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).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.

To study the development of changes for Raf kinase inhibitor protein (RKIP) and its mRNA in rats hippocampus after electromagnetic radiation.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.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.The down-regulation of RKIP and its related proteins of hippocampus is induced by electromagnetic radiation.

To explore the effect of IL-11 on the activation of Jak/STAT pathway and the expressions of Bax and Bcl-2 in the intestinal epithelial cells exposed to neutron radiation.The BALB/c mice and IEC-6, irradiated by 4 Gy neutron with or without IL-11 treatment, served as in vivo and in vitro model seperately. The changes of the intestines, activity of Jak1 and STAT3 and expressions of Bax and Bcl-2 were observed by HE staining, Western blot, EMSA, immunohistochemistry and image analysis.(1)Mice exposed to neutron radiation showed severe intestinal damages and no obvious regeneration was seen. IL-11-treated mice had a larger number of cryptal epithelial cells and crypts. (2)Neutron radiation decreased the activities of Jak1 and STAT3, while IL-11 increased their activities. (3) Neutron radiation decreased the expression of Bax and didn't change the level of Bcl-2 in the murine intestine. IL-11 administration decreased the expression of Bax and increased that of Bcl-2.The mechanism of the intestinal protection of IL-11 in neutron irradiation might be that IL-11 stimulation triggered activation of Jak/STAT pathway, downregulated the expression of Bax and upregulated the expression of Bcl-2.

To determine the effect of high power microwave (HPM) radiation on the structure and function of blood-testis barrier (BTB) in rats.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).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.HPM radiation may damage the structure and increase the permeability of BTB.

To study the effects of electromagnetic radiation on RKIP and phosphorylated ERK in primary cultured hippocampus neurons. The inhibitor of MEK U0126 was applied to investigate the role of RKIP mediated ERK pathway in radiation injury.Primary hippocampus neurons were cultured in vitro. X-HPM, S-HPM and EMP were taken as radiation source respectively to establish three cell models exposed to electromagnetic radiation. RKIP and phosphorylated ERK were measured by immunofluorescent labelling and laser scanning confocal microscope. Apoptosis and death fraction of the cells were detected by Annexin V-PI double labelling and flow cytometry.After three kinds of electromagnetic radiation, the expression of RKIP in hippocampus neurons decreased but the expression of phosphorylated ERK increased, and its nuclear translocation occurred. No significant differences were seen between radiation groups. Apoptosis and death fraction of the neurons in U0126 pretreatment groups was significantly lower than that in radiation groups but they were still higher than those in sham-radiation group.The excessive activation of RKIP mediated ERK pathway is one of the important mechanisms for the apoptosis and death of hippocampus neurons induced by electromagnetic radiation. U0126 have some protective effects on radiation injury.

To investigate the effect of microwave radiation on expression and phosphorylation of synapsin I and to discover the mechanism by research on the change of expression of BDNF and its receptor, TrkB.PC12 cells were exposed to microwave with average power density being 30 mW/cm(2). HPLC was used to detect the release of amino acids; RT-PCR, Western blot and immunocytochemistry were used to detect the expressions of synapsin I, BDNF and TrkB; immune co-precipitation was used to study the interaction of BDNF and TrkB.It resulted in the decrease of the release of Asp, Glu, GABA and Gly at 1 h (P0.01) after radiation. Protein of synapsin I was decreased in 9 h-2 d (P0.01 or P0.05); its mRNA was decreased in 3-9 h and increased at 1 d (P0.01 or P0.05); its phosphorylation was decreased at 3 h, increased at 1 d, and decreased at 2 d again (P0.01 or P0.05) after radiation. Protein of BDNF was decreased at 3 h and increased in 1-2 d (P0.01 or P0.05); its mRNA were decreased in 3-9 h, increased at 1d, and decreased at 2 d again (P0.01 or P0.05) after radiation. Protein of TrkB was increased in 3 h-1 d (P0.01 or P0.05); its mRNA decreased at 3 h and 2 d (P0.01) after radiation. The interaction between BDNF and TrkB was increased in 3-9 h, but decreased in 1-2 d (P0.01 or P0.05) after radiation.Microwave radiation can induce the decrease of the release of amino acids and the expression and phosphorylation of synapsin I, and the abnormality of expressions and interaction of BDNF and TrkB in PC12 cells. The factors might play a role in the injury and repair of information transmission in PC12 cells.

Radiation pulmonary fibrosis (RPF) is characterized by fibroblast proliferation and excessive accumulation of extracellular matrix (ECM). Transforming growth factor beta (TGFbeta) is a switch factor in the initiation and development of RPF and serves as a therapeutic target. Blocking TGFbeta1 signal transduction pathway might alleviate RPF. This study was to investigate the effects of two Smad pathway inhibitors, SB203580 and WP631, on Smad signal transduction pathway in human lung fibroblasts (HLFs) after irradiation.HLFs were pretreated with 25 micromol/L SB203580 or 5 nmol/L WP631, then irradiated with 3 Gy 60Co gamma rays and stimulated by 10 microg/L TGFbeta1. The transcriptional activity of SP1 and AP1 were measured using electrophoretic mobility shift assay (EMSA). Expressions of Smad3, Smad4, Smad7, p-Smad3 and P21(WAF1/CIP1) were detected by Western blot. The expression of type Iplasminogen activator inhibitor (PAI-I) was detected by immunohistochemical staining The cell cycle was measured by FACS.After irradiation. with 3 Gy gamma rays and stimulation by TGFbeta1, HLFs pre-incubated with SB203580 or WP631 were increased in G2-M phase and decreased in S phase as compared with cells without pretreatment. p21(WAF1/CIP1) and p-Smad3 were decreased in HLFs pretreated with SB203580, while PAI-1 was decreased in HLFs pretreated with WP631. Furthermore, the transcriptional activity of SP1 and AP1 was inhibited by WP631.SB203580 and WP631 can abrogate excessive proliferation, expressions of p21(WAF1/CIP1) and PAI-1 induced by gamma rays and TGFbeta1 in HLFs through blocking Smad signal transduction pathway.

To observe the effect of neutron radiation on intestinal epithelial cells 6 (IEC-6), to study the effect of IL-2 on the proliferation and recovery of neutron-injured IEC-6, and to investigate the regulatory mechanisms of IL-2 on the injured IEC-6.4Gy-neutron-injured IEC-6 were treated by IL-2, with or without the blocking agent JAK(1) (A77-1726). The change of proliferative activity and death manner of the treated IEC-6 were detected by MTT colorimetry and flow cytometry at 10, 15, 30 minutes and 1, 3, 6, 12, 24, 48, 72 hours respectively. The expression of IL-2Rbeta and the activation of JAK(1) of neutron-injured IEC-6 treated by IL-2 were detected by immunocytochemical stainning and Western blot.After IEC-6 were radiated by 4 Gy neutron for 24 hours, the proliferative activity of IEC-6 decreased markedly but increased strikingly after IL-2 treatment (P0.05). The apoptosis of IEC-6 in IL-2-treated group decreased (P0.05), but there was no obvious difference in necrotic cell number. After neutron-injured IEC-6 were treated by IL-2, JAK(1) was activated at 10 and 15 minutes, and the expression of IL-2Rbeta increased apparently at 24 hours. When treated by JAK(1) and IL-2, the proliferative activity of neutron-injured IEC-6 was much lower than that in IL-2-treated group.IL-2 can accelerate the proliferation of neutron-radiated IEC-6 and protect them from neutron injury. IL-2Rbeta and JAK(1) participate in the regulation of neutron-injured IEC-6 by IL-2.

To investigate the effect of microwave radiation on synaptic structure, characteristic of synaptosome, the contents and release of neurotransmitters in hippocampus in Wistar rats.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.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 (P0.01) and tc of membrane proteins (P0.01) of synaptosome increased contents of glutamic acid and glycine (P0.01) and release of GABA increased the increase of contents and release of acetylcholine, and activity of acetyl cholinesterase (P0.01) increased.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.

To investigate the effects of (60)Co gamma rays on the biological behaviour of lung fibroblasts (LFs) in C57BL/6J and C3H/HeN mice.LFs in C57BL/6J and C3H/HeN mice were isolated, cultured and irradiated by 2, 4, 6 and 8 Gy (60)Co gamma rays. The proliferative activity and cell cycle were detected by MTT colorimetry, AgNOR staining and fluorescence-activated cell sorting(FACS). Then the expressions of alpha-smooth muscle actin (a-SMA), matrix metal proteinase (MMP-1) and tissue inhibitor of metalloproteinase (TIMP-1) in LFs were observed by immunocytochemical staining.The proliferation of LFs in C57BL/6J mice was not promoted by 2, 4, 6 and 8 Gy (60)Co gamma rays, but the number of aneuploid cells increased. MMP-1 was weak positive. The expression of a-SMA and TIMP-1 was enhanced by (60)Co gamma rays. The proliferation of LFs in C3H/HeN mice was not promoted by 2, 4, 6 and 8 Gy (60)Co gamma rays either, but the number of cells in G2-M phase increased. The expression of MMP-1 and TIMP-1 was enhanced, but the expression of a-SMA was decreased by (60)Co gamma rays.The biological behaviours of the irradiated LFs in C57BL/6J and C3H/HeN mice are different. LFs in C57BL/6J mice can be pactivatedq. Our study will provide a celluar basis for the researches into the C57BL/6J mice which are prone to radiation pulmonary fibrosis (RPF).

To explore the injury effect and mechanism of hypothalamic neurons after high power microwave (HPM) exposure.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.The ratio of apoptosis was significantly higher than that of the sham exposure (P0.05) induced by 10 and 30 mW/cm(2) HPM and necrosis increased significantly (P0.05) 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 (P0.01) while MMP decreased significantly (P0.01) after radiation of 30 mW/cm(2) HPM at 6 h after exposure.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.

To explore the pathological characteristics and the dynamic change regularity of the testis induced by high power microwave (HPM) radiation.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.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 (P0.01 or P0.05).HPM radiation may cause injury of testicular spermatogenic cells in rats, which has a positive correlation to radiation dosage and time.

To explore the effect of recombinant human interleukin-11 (rhIL-11) on the expressions of interleukin-11 receptor alpha-chain (IL-11Ralpha) and an additional signal transducer glycoprotein 130 (gp130) in intestinal epithelium cell line-6 (IEC-6) after neutron irradiation.Cultured IEC-6 cells were exposed to 4.0Gy neutron and treated with 100 ng/mL rhIL-11 12 h prior to or immediately after irradiation. The apoptosis and necrosis rates and expressions of IL-11Ralpha and gp130 were observed by flow cytometry, immunohistochemistry, Western blot and image analysis.The apoptosis rate of IEC-6 cells was increased by irradiation at 6 h (P0.01), IL-11 stimulation resulted in a decreased apoptosis rate in irradiated IEC-6 cells (P0.05). In normal control IEC-6 cells, intense immunoreactivity of IL-11Ralpha was located within the cell membrane and cytoplasm. The level of IL-11Ralpha expression significantly decreased at 6 h after irradiation (P0.01) and restored at 24 h after irradiation. In IEC-6 cells treated with both radiation and rhIL-11, the level of IL-11Ralpha expression was higher than that of irradiated cells (P0.05). When it came to gp130 protein, it was located in the cytoplasm of IEC-6 cells. After irradiation, we found a progressive decrease in the expression of gp130 protein (P0.05) in 48 h post-radiation, while in rhIL-11-stimulated cells, it came back to normal level at 24 h after irradiation and decreased at 48 h, but was still higher than that of only irradiated cells (P0.05).rhIL-11 can protect IEC-6 cells from neutron irradiation. The protective effect of rhIL-11 might be connected with its ability to up-regulate the expressions of specific ligand-binding subunit IL-11Ralpha and signal-transducing subunit gp130.

To investigate the effects of TGFbeta1 on the transcriptive activity of SP1, AP1 and Smad3-Smad4 in rat lung fibroblasts(RLF).RLFs were isolated and cultured and then treated with 10 microg/L TGFbeta1. The transcriptive activity of SP1, AP1 and Smad3-Smad4 and the expression of plasminogen activator inhibitor I(PAI-1) and collagen I were detected by means of electrophoretic mobility shift assay (EMSA), Western blot and immunohistochemical staining.After treatment with 10 microg/L TGFbeta1, AP1, SP1 and Smad3-Smad4 were activated and the expression of collagen I and PAI-1 were increased.TGFbeta1 may activate SP1, AP1 and Smad3-Smad4 and thus increase the expression of PAI-1 and collagen I.

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.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.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, P0.05). beta(1)-AR expression in endocardium, membrane and cytoplasm of myocardium of left ventricle was increased on d1 after radiation, peaked on d3 (P0.05) and recovered on d14. M(2)-AchR expression was peaked on d1 (P0.01) and recovered on d14.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.

To observe the effect of ionizing radiation on intestinal epithelial cells 6 (IEC-6) and the effect of IL-2 on the proliferation and recovery of radiation-injured IEC-6 cells.IEC-6 cells exposed to 4, 8 and 12 Gy gamma ray were analyzed with MTT colorimetry, light microscopy, electron microscopy, DNA gel electrophoresis and flow cytometry at 3, 6, 9, 12 hours and 1, 2, 3 days after radiation. Proliferation of 8 Gy gamma ray-irradiated IEC-6 cells which was treated with IL-2 was detected by MTT colorimetry at 3, 6, 9, 12 and 24 hours after irradiation.Proliferation of IEC-6 decreased with the increased dose of gamma ray radiation. Apoptotic IEC-6 cells increased apparently at 24 hours after radiation with 8.0 Gy gamma ray, IL-2 could enhance the proliferation of irradiated IEC-6 cells (especially at concentration of 1 x 10(5) U/L) in a dose-dependent manner.4-12 Gy of gamma ray radiation can reduce the proliferation and cause apoptosis of IEC-6 cells. IL-2 can accelerate proliferation of irradiated IEC-6 cells and protect IECs from ionization radiation injury.

To investigate the characteristics and mechanism of the acute and chronic injuries induced by unsymmetrical dimethylhydrazine (UDMH).A total of 128 male rats were randomly divided into four groups: UDMH intoxication acute response group and chronic response group, and corresponding control groups. UDMH was administrated through inhalation at the concentration of 8x10(-4)g/m(3) for 15 minutes. Animals of each group were sacrificed at 3, 6, 12, 24, 48 and 72 hours respectively after the intoxication. Pathologic changes and blood gas were examined. Chronic injuries and pathologic changes were also observed 1 year after the intoxication.Major pathological changes in the intoxication group were cerebral edema, degeneration and necrosis of neuron, enlargement and hemorrhage of capillary. Damages of different degree were found in liver, kidney, lung, heart, spleen, stomach, intestine, thymus, blood, bone marrow. Pallium ischemia was also found in the intoxicated rats 1 year after the intoxication, including ischemia damage of neuron in cerebral cortex, hemorrhage and focal liquefaction of thalamus and medulla conducting bind, dissociation, rupture, not uniform circuitry in conducting fibers.Our study reveals the basic pathological induced by intoxication of UDMH. The most severe stage of the injury appears 2-6 hours after intoxication. Long term investigation reveals pallium ischemia, thalamus hemorrhage and liquefaction in the medulla oblongata 1 year after the intoxication with UDMH. All the changes are significant.