A new predictor of coronary artery disease in acute ischemic stroke or transient ischemic attack patients: pericarotid fat density.

OBJECTIVES: The study aims to evaluate the incremental predictive value of pericarotid fat density (PFD) on head and neck computed tomography angiography (CTA) for the obstructive coronary artery disease (CAD) (≥ 50% stenosis) relative to a clinical risk model (Framingham risk score (FRS)) and the degree of carotid artery stenosis and plaque type in acute ischemic stroke (AIS) or transient ischemic attack (TIA) patients without a known history of CAD. METHODS: In a cohort of 134 consecutive stable patients diagnosed with AIS or TIA undergoing head and neck CTA between January 2010 and December 2021, pericarotid adipose tissue density (PFD) was quantified using a dedicated software. We collected demographic and clinical data, assessed the risk of CAD using the FRS, and analyzed coronary and carotid artery CTA images. Univariate and multivariate logistic regression analyses were performed to assess associations between FRS, PFD, CTA variables, and obstructive CAD risk. Four prediction models were established to evaluate the incremental predictive value of PFD relative to FRS, stenosis degree, and plaque types. Receiver operating characteristic (ROC) curves were generated, and the areas under the curves (AUC) were compared. RESULTS: Increasing FRS, stenosis degree, and PFD values were positively correlated with obstructive CAD (all p < 0.05). In the predictive models for obstructive CAD, the model incorporating carotid stenosis exhibited superior predictive performance compared to FRS alone (p < 0.05). Moreover, the predictive model integrating PFD demonstrated enhanced performance and yielded the highest AUC of the receiver operator characteristic curve (AUC = 0.783), with sensitivity and specificity values of 86.89% and 65.75%, respectively. CONCLUSION: CTA-derived PFD measurements offer supplementary predictive value for obstructive CAD beyond FRS and stenosis, thereby facilitating improved risk stratification of TIA or stroke patients without a history of CAD history. CLINICAL RELEVANCE STATEMENT: CTA-derived PFD provides incremental predictive value for obstructive coronary artery disease in acute ischemic stroke or transient ischemic attack patients without CAD history, beyond Framingham risk score and carotid artery stenosis degree, improving risk stratification. KEY POINTS: • Pericarotid fat density is associated with obstructive coronary artery disease in acute ischemic stroke or transient ischemic attack patients. • Higher pericarotid fat density corresponds to an increased risk of obstructive coronary artery disease. • Estimation of pericarotid fat density using computed tomography angiography imparts additional predictive value for obstructive CAD in risk stratification of acute ischemic stroke or transient ischemic attack patients.

An updated meta-analysis of partial splenic embolization versus splenectomy in the treatment of hypersplenism due to cirrhosis.

OBJECTIVE: To evaluate the efficacy and safety of partial splenic embolization (PSE) versus splenectomy (SP) for hypersplenism. MATERIAL AND METHODS: Pubmed, Embase, Cochrane Library, China National Knowledge Infrastructure (CNKI), Wanfang, and Chinese Science and Technology Periodical Database (VIP) databases were systematically searched to identify all relevant studies. Stratified meta-analysis was also conducted to control the influence of confounding factors on the research results. RESULTS: Twenty-three studies comparing PSE with SP involving a total of 1849 hypersplenism patients were selected. Postoperative increased level of platelet (PLT) [mean difference (MD) = -65.51; 95% confidence interval (CI), -81.33 to -41.69; p < .00001] were better in SP than in PSE; however, PSE was associated with less operation time (MD = -53.47; 95% CI, -65.01 to -41.94; p < .00001), less intraoperative blood loss (MD = -61.58; 95% CI, -80.35 to -42.82; p < .00001), shorter hospital stay (MD = -2.98;95% CI, -4.07 to -1.88; p < .00001) and lower complication rate [odds ratio (OR) = 0.53; 95% CI, 0.32 to 0.90; p = .02] compared with the SP. Meanwhile, there was no significant difference in postoperative increased level of white blood cells (WBC) (MD = -1.02; 95% CI, -2.16 to 0.11; p = .08) and postoperative increased level of hemoglobin (HB) (MD = -4.09; 95% CI, -14.06 to 5.88; p = .42) between PSE and SP group. CONCLUSION: PSE had similar efficacy with SP in improving postoperative PLT, WBC, and HB levels. Moreover, PSE had the advantages of less trauma and fewer complications as well as faster recovery when compared with SP. Therefore, we tended to be cautious about SP and considered that patients with hypersplenism might benefit more from PSE.

Insertion of I-125 seed-loaded stent for inoperable hilar cholangiocarcinoma.

INTRODUCTION: Stent insertion is the most frequently used option to treat malignant biliary obstruction (MBO) patients. Hilar cholangiocarcinoma (HCCA) is the most common disease that causes hilar MBO. AIM: To assess the clinical efficacy and long-term outcomes of I-125 seed-loaded stent (ISS) insertion for HCCA patients. MATERIAL AND METHODS: Consecutive patients with HCCA underwent either normal stent (NS) or ISS insertion between January 2017 and December 2019. The baseline and treatment data of these two groups were compared. RESULTS: During the period, a total of 93 patients with inoperable HCCA were divided into either NS (n = 48) or ISS (n = 45) insertion groups at our centre. Technical success rates of the NS and ISS insertion were 91.7% and 95.6%, respectively (p = 0.733). Clinical success rates were 93.2% and 100% in the NS and ISS groups, respectively (p = 0.24). Stent dysfunction was observed in 11 and 8 patients in the NS and ISS groups, respectively (p = 0.47). The median stent patency was 143 days and 208 days in the NS and ISS groups, respectively (p < 0.001). All patients died in the follow-up period, with median survival duration of 178 days and 220 days in the NS and ISS groups, respectively (p < 0.001). ISS insertion was the only predictor of longer patency (p = 0.002) and survival (p = 0.01). CONCLUSIONS: ISS insertion might achieve longer patency and overall survival in patients with inoperable HCCA as compared with NS insertion.

Neuroprotective and Anti-Inflammatory Effect of Pterostilbene Against Cerebral Ischemia/Reperfusion Injury via Suppression of COX-2.

Background: The incidence of cerebral ischemia disease leading cause of death in human population worldwide. Treatment of cerebral ischemia remains a clinical challenge for researchers and mechanisms of cerebral ischemia remain unknown. During the cerebral ischemia, inflammatory reaction and oxidative stress plays an important role. The current investigation scrutinized the neuroprotective and anti-inflammatory role of pterostilbene against cerebral ischemia in middle cerebral artery occlusion (MCAO) rodent model and explore the underlying mechanism. Methods: The rats were divided into following groups viz., normal, sham, MCAO and MCAO + pterostilbene (25 mg/kg) group, respectively. The groups received the oral administration of pterostilbene for 30 days followed by MCAO induction. The neurological score, brain water content, infarct volume and Evan blue leakage were estimated. Hepatic, renal, heart, inflammatory cytokines and inflammatory mediators were estimated. Results: Pterostilbene treatment significantly (p < 0.001) improved the body weight and suppressed the glucose level and brain weight. Pterostilbene significantly (p < 0.001) reduced the hepatic, renal and heart parameters. Pterostilbene significantly (p < 0.001) decreased the level of glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD) and decreased the level of malonaldehyde (MDA), 8-Hydroxy-2'-deoxyguanosine (8-OHdG). Pterostilbene significantly (p < 0.001) inflammatory cytokines and inflammatory parameters such as cyclooxygenase-2 (COX-2), inducible nitric oxidase synthase (iNOS) and prostaglandin (PGE2). Pterostilbene significantly (p < 0.001) down-regulated the level of metalloproteinases (MMP) such as MMP-2 and MMP-9. Pterostilbene suppressed the cellular swelling, cellular disintegration, macrophage infiltration, monocyte infiltration and polymorphonuclear leucocyte degranulation in the brain. Conclusion: In conclusion, Pterostilbene exhibited the neuroprotective effect against cerebral ischemia in rats via anti-inflammatory mechanism.

Results Obtained with the Protege EverFlex Self-expanding Bare Stent in Interventional Treatment of Spontaneous Isolated Visceral Artery Dissection.

OBJECTIVE: We evaluated the early and midterm results of the endovascular approach with a certain type of bare stent to treat spontaneous isolated visceral artery dissection (SIVAD). METHODS: 28 patients with symptomatic SIVAD were selected from two hospitals from July 2014 to September 2020. All patients had symptoms of acute persistent abdominal pain accompanied by varying degrees of nausea and vomiting. The diagnosis of SIVAD was made according to the multidetector CT angiography (CTA) findings. We retrospectively analyzed the patients' medical records. According to our previous clinical experience, the Protege EverFlex self-expanding bare stent was used in these patients, and we subsequently followed up the patients to record and analyze their outcomes after surgery. The imaging results before and after the operations were compared. RESULTS: All 28 patients were successfully implanted with Protege EverFlex stents. The true lumen blood flow of the SIVAD recovered during the operation. The residual stenosis rate was less than 30%, and the technical success rate was 100%. There were no complications, such as bleeding, intestinal necrosis, digestive tract perforation, liver failure or spleen infarction. The abdominal pain was relieved or eliminated in all patients. CONCLUSION: The Protege EverFlex self-expanding bare stent and the endovascular approach could be a minimally invasive, safe and effective treatment method for SIVAD with a high success rate and a relatively low price.

AMPKα1 overexpression improves postoperative cognitive dysfunction in aged rats through AMPK-Sirt1 and autophagy signaling.

Postoperative cognitive dysfunction (POCD) is a common complication in elderly patients who undergo surgery involving anesthesia. Its underlying mechanisms remain unclear. Autophagy plays an important role in the damage and repair of the nervous system and is associated with the development of POCD. Using a rat model, adenosine monophosphate-activated protein kinase α1 (AMPKα1), an important autophagy regulator, was found to be significantly downregulated in rats with POCD that was induced by sevoflurane anesthesia or by appendectomy. Overexpression of AMPKα1-ameliorated POCD, as indicated by decreased escape latencies and increased target quadrant swimming times, swimming distances, and platform crossing times during Morris water maze tests. AMPKα1 overexpression activated autophagy signals by increasing the expression of light chain 3 II (LC3-II) and Beclin1 and decreasing the expression of p62 in the hippocampus of rats with POCD. Moreover, blocking autophagy by 3-methyladenine partly attenuated AMPKα1-mediated POCD improvement. Furthermore, overexpression of AMPKα1 could upregulate the expression of p-AMPK and Sirt1 in the hippocampus of rats with POCD. Intriguingly, inhibiting AMPK signals via Compound C effectively attenuated AMPKα1-mediated POCD improvement, concomitant with the downregulation of p-AMPK, Sirt1, LC3-II, and Beclin1 and the upregulation of p62. We thus concluded that overexpression of AMPKα1 can improve POCD via the AMPK-Sirt1 and autophagy signaling pathway.

Rutin ameliorates diabetic neuropathy by lowering plasma glucose and decreasing oxidative stress via Nrf2 signaling pathway in rats.

Rutin exhibits antidiabetic, antioxidant and anti-inflammatory properties, which makes rutin an attractive candidate for diabetic complications. The present study was designed to investigate the potential effect of rutin on diabetic neuropathy. After induction of diabetic neuropathy, rutin (5mg/kg, 25mg/kg and 50mg/kg) were daily given to the diabetic rats for 2 weeks. At the end of rutin administration, rutin produced a significant inhibition of mechanical hyperalgesia, thermal hyperalgesia and cold allodynia, as well as partial restoration of nerve conduction velocities in diabetic rats. Furthermore, rutin significantly increased Na(+), K(+)-ATPase activities in sciatic nerves and decreased caspase-3 expression in dorsal root ganglions (DRG). In addition, rutin significantly decreased plasma glucose, attenuated oxidative stress and neuroinflammation. Further studies showed that rutin significantly increased hydrogen sulfide (H2S) level, up-regulated the expression of nuclear factor-E2-related factor-2 (Nrf2) and heme oxygenase-1 (HO-1) in DRG. The evidences suggest the beneficial effect of rutin on diabetic neuropathy. Additionally, insulin (2 IU) and BG-12 (15mg/kg) were used to investigate the mechanisms underlying the beneficial effect of rutin on diabetic neuropathy. Insulin achieved lower plasma glucose and BG-12 achieved comparable Nrf2 expression than/to rutin (50mg/kg), respectively. In contrast, the beneficial effect of insulin and BG-12 was inferior to that of rutin (50mg/kg), suggesting that both lowered plasma glucose and Nrf2 signaling contribute to the beneficial effect of rutin on diabetic neuropathy. In conclusion, rutin produces significant protection in diabetic neuropathy, which makes it an attractive candidate for the treatment of diabetic neuropathy.

Growth inhibitory effect of adenovirus-mediated tissue-targeted expression of ribosomal protein L23 on human colorectal carcinoma cells.

A large body of evidence has established murine double minute 2 (MDM2) as a crucial negative regulator of p53 and the major suppressor of p53 function in tumors with wild-type (wt)-p53. Therefore, by inhibiting MDM2 one may reactivate p53 in tumor cells, leading to their demise. Previous studies revealed that ribosomal protein L23 (RPL23) inhibited MDM2-mediated p53 ubiquitination through direct binding to MDM2, and subsequently induced the p53 level as well as its activity, suggesting that it may be a candidate for use in tumor gene therapy. In the present study, we developed a recombinant adenoviral vector expressing the RPL23 gene under control of the carcinoembryonic antigen (CEA) promoter (rAd/CEA-RPL23), and using an in vitro system with cultured human colorectal carcinoma LoVo cells harboring the wt-p53 gene, we proved that rAd/CEA-RPL23 infection could induce the accumulation of endogenous wt-p53 protein and thus lead to the inhibition of tumor cell growth via inducing cell cycle arrest and apoptosis. In vivo treatment of rAd/CEA-RPL23 also exhibited a significant inhibitory effect on tumor growth in nude mice bearing LoVo xenografts. Furthermore, we showed that rAd/CEA-RPL23 synergized with classic chemotherapeutic agent 5-fluorouracil (5-FU) and enhanced its activity against LoVo cells in vivo and in vitro. Taken together, the data presented here suggest that CEA promoter-targeted exogenous RPL23 expression could be of therapeutic value against human colorectal carcinoma that retains wt-p53.

Pulsed electromagnetic wave exposure induces ultrastructural damage and upregulated expression of heat shock protein 70 in the rat adenohypophysis.

The aim of the present study was to investigate the ultrastructural damage and the expression of heat shock protein 70 (HSP70) in the rat adenohypophysis following pulsed electromagnetic wave (PEMW) exposure. The rats were randomly divided into four groups: Sham PEMW exposure, 1 x 10(4) pulses of PEMW exposure, 1 x 10(5) pulses of PEMW exposure and 3 x 10(5) pulses of PEMW exposure. Whole body radiation of 1 x 10(4) pulses, 1 x 10(5) pulses and 3 x 10(5) pulses of PEMW were delivered with a field strength of 100 kV/m. The rats in each group (n=6 in each) were sacrificed 12, 24, 48 and 96 h after PEMW exposure. Transmission electron microscopy was then used to detect the ultrastructural changes and immunocytochemistry was used to examine the expression of HSP70. Cellular damage, including mitochondrial vacuolation occurred as early as 12 h after PEMW exposure.More severe cellular damages, including cell degeneration and necrosis, occurred 24 and 48 h after PEMW exposure. The PEMW-induced cellular damage increased as the number of PEMW pulses increased. In addition, the expression of HSP70 significantly increased following PEMW exposure and peaked after 12 h. These findings suggested that PEMW induced ultrastructural damages in the rat adenohypophysis and that HSP70 may have contributed to the PEMW-induced adenohypophyseal damage.

Effects of PEMF exposure at different pulses on osteogenesis of MC3T3-E1 cells.

OBJECTIVE: Pulsed electromagnetic fields (PEMFs) were considered to be a factor which may affect osteogenesis of osteoblasts, but the effects were diverse with different PEMF parameters. The aim of the current study is to explore the effects of exposure to PEMFs at different pulse number on osteogenesis of osteoblasts. DESIGN: The mouse osteoblast-like MC3T3-E1 cells were exposed to 0, 400 or 2800 pulses 400kV/m PEMF and the proliferation, differentiation and mineralization of cells were observed after PEMF exposure by the methods of MTT, biochemical measurement, real-time PCR and Alizarin Red assay. RESULTS: Compared with 0 pulses groups, the growth curve, alkaline phosphatase (ALP) activity, mRNA level of osteocalcin (OCN) and mineralized nodule formation of MC3T3-E1 cells did not change after 400 pulses PEMF exposure, but decreased after 2800 pulses PEMF exposure. It suggested that under our experimental conditions, only 2800 pulses 400kV/m PEMF exposure can suppress the proliferation, differentiation and mineralization of MC3T3-E1 cells, but 400 pulses 400kV/m PEMF exposure cannot. CONCLUSIONS: Pulse number is another involved parameter which may influence the effects of PEMF on osteogenesis of osteoblasts.

Effects of electromagnetic pulse on serum element levels in rat.

Electromagnetic pulse (EMP) was a potentially harmful factor to the human body, and a biological dosimetry to evaluate effects of EMP is necessary. Little is known about effects of EMP on concentration of macro and trace elements in serum so far. In this study, Sprague-Dawley rats were randomly divided into 50-kV/m EMP-exposed group (n = 10), 100-kV/m EMP-exposed group (n = 10), 200-kV/m EMP-exposed group (n = 40), and the sham-exposed group (n = 20). The macro and trace element concentrations in serum were examined at 6, 12, 24, and 48 h after EMP exposure at different electric field intensities. Compared with the sham-exposed groups, the concentration of sodium (Na), potassium (K), magnesium (Mg), calcium (Ca), zinc (Zn), copper (Cu), iron (Fe), selenium (Se), and manganese (Mn) in rat serum was not changed significantly within 48 h after 200 pulses of EMP exposure at electric field intensity of 50, 100, and 200 kV/m although the K level was decreased and the Ca level was increased with the electric field intensity of EMP increasing. In addition, there was a tendency that the Zn level was decreased with the time going on within 48 h after EMP exposure. Under our experimental conditions, EMP exposure cannot affect the concentration of macro and trace elements in rat serum. There was no time-effect or dose-effect relationship between EMP exposure and serum element levels. The macro and trace elements in serum are not suitable endpoints of biological dosimetry of EMP.

A specific miRNA signature promotes radioresistance of human cervical cancer cells.

BACKGROUND: The mechanisms responsible for cervical cancer radioresistance are still largely unexplored. The present study aimed to identify miRNAs associated with radioresistance of cervical cancer cells. METHODS: The radioresistant cervical cancer cell variants were established by repeated selection with irradiation. The miRNA profiles of radioresistant cells and their corresponding controls were analyzed and compared using microarray. Differentially expressed miRNAs were confirmed by quantitative real-time PCR. Cervical cancer cells were transfected with miRNA-specific mimics or inhibitors. Radiosensitivity of cervical cancer cells were determined using colony-forming assay. RESULTS: Among the differentially expressed miRNAs, 20 miRNAs showed the similar pattern of alteration (14 miRNAs were overexpressed whilst 6 were suppressed) in all three radioresistant cervical cancer cell variants compared to their controls. A miRNA signature consisting of 4 miRNAs (miR-630, miR-1246, miR-1290 and miR-3138) exhibited more than 5 folds of increase in radioresistant cells. Subsequent analysis revealed that these four miRNAs could be up-regulated in cervical cancer cells by radiation treatment in both time-dependent and dose-dependent manners. Ectopic expression of each of these 4 miRNAs can dramatically increase the survival fraction of irradiated cervical cancer cells. Moreover, inhibition of miR-630, one miRNA of the specific signature, could reverse radioresistance of cervical cancer cells. CONCLUSIONS: The present study indicated that miRNA is involved in radioresistance of human cervical cancer cells and that a specific miRNA signature consisting of miR-630, miR-1246, miR-1290 and miR-3138 could promote radioresistance of cervical cancer cells.

Effect of Electromagnetic Pulses (EMP) on associative learning in mice and a preliminary study of mechanism.

PURPOSE: To investigate the effects of electromagnetic pulses (EMP) on associative learning in mice and test a preliminary mechanism for these effects. MATERIALS AND METHODS: A tapered parallel plate gigahertz transverse electromagnetic (GTEM) cell with a flared rectangular coaxial transmission line was used to expose male BALB/c mice to EMP (peak-intensity 400 kV/m, rise-time 10 ns, pulse-width 350 ns, 0.5 Hz and total 200 pulses). Concurrent sham-exposed mice were used as a control. Associative learning, oxidative stress in the brain, serum chemistry and the protective action of tocopherol monoglucoside (TMG) in mice were measured, respectively. RESULTS: (1) Twelve hour and 1 day post EMP exposure associative learning was reduced significantly compared with sham control (p<0.05) but recovered at 2 d post EMP exposure. (2) Compared with the sham control, lipid peroxidation of brain tissue and chemiluminescence (CL) intensity increased significantly (p<0.05), while the activity of the antioxidant enzymes Superoxide Dismutase [SOD], Glutathione [GSH], Glutathione Peroxidase [GSH-Px], Catalase [CAT]) decreased significantly (p<0.05) at 3 h, 6 h, 12 h and 1 d post EMP exposure. All these parameters recovered at 2 d post EMP exposure. (3) No significant differences between the sham control group and EMP exposed group were observed in serum cholesterol and triglycerides. (4) Pretreatment of mice with TMG showed protective effects to EMP exposure. CONCLUSIONS: EMP exposure significantly decreased associative learning in mice and TMG acted as an effective protective agent from EMP exposure. This mechanism could involve an increase of oxidative stress in brain by EMP exposure.

The effects of electromagnetic pulses (EMP) on the bioactivity of insulin and a preliminary study of mechanism.

PURPOSE: To investigate the effects of electromagnetic pulse (EMP) exposure on the bioactivity of insulin and a preliminary mechanism for these effects. MATERIALS AND METHODS: A tapered parallel plate Gigahertz Transverse Electromagnetic (GTEM) cell with a flared rectangular coaxial transmission line was used to expose the insulin solution to EMP. Concurrent sham-exposed insulin solutions were used as a control. The effect of EMP-exposed insulin on fasting blood glucose levels of type I diabetes model mice, the effect of EMP on binding affinity between insulin and its receptor and the effect of EMP on insulin's fluorescence intensity were detected, respectively. RESULTS: (i) After EMP exposure, compared with sham-exposed insulin, the bioactivity of insulin in decreasing fasting blood glucose levels in type I diabetes model mice was reduced significantly (p = 0.023). (ii) Compared with sham-exposed insulin group, the percentage fluorescein isothiocyannate (FITC) labelling of HL-7702 cells was significantly reduced in the EMP-exposed insulin group (22.7-13.8%, respectively). (iii) Compared with sham-exposed insulin, the fluorescence intensity was significantly reduced in EMP-exposed insulin (p < 0.001). CONCLUSIONS: EMP exposure significantly decreased the bioactivity of insulin to reduce the blood glucose levels in type I diabetic mice. This could be due to a decreased binding affinity between insulin and its receptor. This mechanism could involve an alteration of insulin's' conformation caused by EMP exposure.

[Effects on structure and secretion of pituitary gland in rats after electromagnetic pulse exposure].

OBJECTIVE: To investigate the exposure effect of electromagnetic pulse (EMP) on the structure and secretion of pituitary gland in rats. METHODS: Forty-eight male SD rats were randomly divided into eight groups. Four groups were subject to the EMP exposure of 200 kV/m and the others received a sham exposure. At different time points (12, 24, 48 & 96 h) post-exposure, the pathological changes of pituitary gland were observed by light and transmission electron microscope. And the serum levels of prolactin (PRL), growth hormone (GH), adrenocorticotropic hormone (ACTH), thyroid stimulating hormone (TSH) and luteinizing hormone (LH) were measured dynamically by radioimmunoassay. RESULTS: At 12 h post-exposure, swollen mitochondria with cristae loss, dilatation of Golgi complex and diffusive lysosomes were found in endocrine cells of pituitary gland. The above changes became gradually worse. Mitochondrial vacuolization, the formation of myelin figures, distinct dilatation of endoplasmic reticulum, the occurrence of numerous secondary lysosomes and the clustering of heterochromatin under the nuclear membranes could be observed at 48 h. These lesions were alleviated to some degree at 96 h. The serum levels of PRL and ACTH both increased significantly at 12 h (P < 0.01, P < 0.05) and returned to normal at 24 h. The level of GH decreased significantly at 12 h and then returned gradually to normal at 48 h. The level of TSH decreased at 12 h and reached the lowest point at 24 h, then returned to normal at 96 h. LH increased significantly from 24 h to 96 h. CONCLUSION: The EMP exposure of 200 kV/m may induce the changes of the structure and secretion of pituitary gland in rats.

[Change of chart genes expression in small intestines of mouse induced by electromagnetic pulse irradiation].

OBJECTIVE: To explore the bio-effects of electromagnetic pulse(EMP) on mouse small intestines induced by means of gene chip. METHODS: Twelve BALB/c mice were randomly assigned to the normal control group and the EMP group with 6 in each group. The EMP group was irradiated with 200 kV/m, 200 pulses EMP. 18 hours after the irradiation, the mice were sacrificed and their jejunum of small intestines were eviscerated. The fluorescent cDNA probes labeled with Cy3 and Cy5 were prepared from RNA extracted from the intestines of the two groups. Probes of the two groups were then hybridized against cDNA gene chip, the fluorescent signals were scanned with a scanner and the results were analyzed by computer. RESULTS: Compared with the control, 56 genes in gene expression profile were altered. The expression levels of 37 genes were up-regulated distinctly while 19 genes were down-regulated significantly. Among the 56 genes, 19 were reported with known or inferred functions, 12 up-regulated genes were catenin alpha 1 (alpha-catenin), ly-6 alloantigen(Ly-6E), fructose-6-phosphate transaminase (GF6P), ribosomal protein S17 (rpS17), small proline-rich protein 2A (Sprr2a), glandular kallikrein27 (GK27), lipoxygenase-3, aldo-keto reductase (Akr1c12), GSG1, amylase 2 (Amy2),elastase 2, p6-5 gene and 7 down-regulated genes were junctional adhesion molecule (Jam), protein arginine methyltransferase (Carm1),NNP-1, 2-5 A synthetase L2,Mlark gene, ATP synthase alpha subunit, uncoupling protein-2 (Ucp2) gene; the other 37 were reported with unknown functions. CONCLUSION: EMP irradiation could induce specific expressions of some genes in mouse small intestines and most of these genes were up-regulated ones.

Electromagnetic pulses induce fluctuations in blood pressure in rats.

PURPOSE: To investigate the effects of exposure to electromagnetic pulses (EMP) on functional indices of the cardiovascular system in male Sprague-Dawley rats. MATERIALS AND METHODS: A tapered parallel plate Gigahertz Transverse Electromagnetic cell (GTEM cell) with a flared rectangular coaxial transmission line was used to expose the rats to EMP (0.5 pps, total 200 pulses and whole-body averaged specific absorption rate 50 mW/kg at 200 kV/m or 75 mW/kg at 400 kV/m). Concurrent sham-exposed animals were used as controls. Cardiovascular functions, namely, heart rate, and systolic, mean and diastolic blood pressures were measured immediately and up to 4 weeks post-exposure using a non-invasive tail-cuff photoelectric sensor sphygmomanometer. RESULTS: The heart rates in sham- and EMP-exposed rats were not significantly changed. In the exposed rats, increased systolic blood pressure (SBP) occurred at 0 h and decreased SBP occurred at 1 day and 3 days after exposure. Significantly higher diastolic blood pressure (DBP) was found at 0 h and significantly lower DBP was found at 12 h, 1 day, and 1 month after exposure. Significantly higher mean arterial pressure (MAP) was noted at 0 h and significantly lower MAP was noted at 1 day. CONCLUSIONS: Significant alterations in arterial blood pressure were observed in rats exposed to EMP exposure while heart rate was not altered.

Mechanism of exogenous nucleic acids and their precursors improving the repair of intestinal epithelium after gamma-irradiation in mice.

AIM:To clone expressed genes associated with repair of irradiation-damaged mice intestinal gland cells treated by small intestinal RNA, and to explore the molecular mechanism of exogenous nucleic acids improving repair of intestinal crypt.METHODS:The animal mode of test group and control group was established, forty-five mice being irradiated by gamma ray were treated with small intestinal RNA as test group, forty mice being irradiated by gamma ray were treated with physiological saline as control group,five mice without irradiation were used as normal control, their jejunal specimens were collected respectively at 6h, 12h,24h, 4d and 8d after irradiation. Then by using LD-PCR based on subtractive hybridization, these gene fragments differentially expressed between test group and control group were obtained, and then were cloned into T vectors as well as being sequenced. Obtained sequences were screened against. GeneBank, if being new sequences, they were submitted to GeneBank.RESULTS:Ninety clones were associated with repair of irradiation-damaged intestinal gland cells treated by intestinal RNA. These clones from test group of 6h, 12h, 24h, 4d and 8d were respectively 18, 22, 25, 13, 12. By screening against GeneBank, 18 of which were new sequences, the others were dramatically similar to the known sequences, mainly similar to hsp, Nmi,Dutt1, alkaline phosphatase, homeobox, anti-CEA ScFv antibody, arginine/serine kinase and BMP-4,repA. Eighteen gene fragments were new sequences,their accept numbers in GeneBank were respectively AF240164-AF240181.CONCLUSION:Ninety clones were obtained to be associated with repair of irradiation damaged mice intestinal gland cells treated by small intestinal RNA, which may be related to abnormal expression of genes and matched proteins of hsp, Nmi, Dutt1, Na, K-ATPase,alkalineph-osphatase, glkA, single stranded replicative centromeric gene as well as 18 new sequences.