Antagonistic effect of microwave on hematopoietic damage of mice induced by gamma-ray irradiation / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate antagonistic effect of microwave on hematopoietic damage of mice induced by gamma-ray irradiation.</p><p><b>METHODS</b>Male healthy Kunning mice were treated with low dose microwave radiation before exposure to (60)Co gamma-ray irradiation of 8.0 Gy. The 30-day survival rate and average survival time of the mice after the treatment were examined. Peripheral blood parameters and the organ indexes of thymus and spleen were also observed in the irradiated mice. After exposure to 5.0 Gy gamma irradiation, indexes of hematopoietic foci formation of bone marrow cells (CFU-GM) and the proliferation activity of BMNCs were examined. The serum concentration of hemopoietic factors (GM-CSF and IL-3) were detected by ELISA kits.</p><p><b>RESULTS</b>Pre-exposure with 120 microW/cm(2) 900 MHz microwave increased the 30-day survival rate (P < 0.05) and the number of white blood cells of gamma-ray treated mice. The increases of the organ indexes of thymus and spleen, proliferation activity of BMNCs and CFU-GM hematopoietic foci numbers, as well as the higher serum concentration of GM-CSF and IL-3 were observed in the microwave pre-exposure group.</p><p><b>CONCLUSION</b>Low dose microwave radiation may exert potential antagonistic effects on hematopoietic injuries induced by ionizing radiation. The underlying mechanisms might be related with stimulation of hematopoietic growth factors expression, promotion of HSCs/HPCs proliferation, suppression on the reduction of HSCs/HPCs caused by (60)Co gamma-ray, and enhanced construction of the hematopoietic system.</p>

The effect of entecavir treatment on HBV-specific immunity in patient with chronic hepatitis B and its relationship to HBeAg sero-conversion / 中华实验和临床病毒学杂志

<p><b>OBJECTIVE</b>To investigate the effect of Entecavir treatment on HBV-specific immunity in patient with chronic hepatitis B and its relationship to HBeAg sero-conversion.</p><p><b>METHODS</b>Serum aminotransferase (ALT), HBV DNA and HBeAg were monitored before the after entecavir treatment. At the same time point, HBV-specific T cell proliferation was determined by [3H] T-dR incorporation assay, while HBV-specific IFN-alpha secretion was measured by ELISA.</p><p><b>RESULTS</b>The level of HBV DNA and ALT was significantly decreased after entecavir treatment. Same is the titer of HBeAg. In addition, HBeAg sero-conversion was observed in some of them, in whom the HBV-specific T cell proliferation and IFN-alpha production were significantly increased.</p><p><b>CONCLUSION</b>Entecavir treatment resulted in increased HBV-specific immunity along with the inhibition of HBV replication.</p>

Roles of the histaminergic receptors in the locus ceruleus in stress-induced carotid baroreflex resetting in rats / 中国应用生理学杂志

<p><b>AIM</b>To explore the roles of H1 and H2 receptors in the locus ceruleus (LC) in the carotid baroreflex (CBR) resetting resulted from foot-shock stress.</p><p><b>METHODS</b>Male SD rats were divided into two groups (n=18) at random: unstressed and stressed group. The latter were subjected to unavoidable electric foot-shock twice daily for a week and each session of foot-shock lasted 2 hours. The left and right carotid sinus regions were isolated from the systemic circulation in all animals anesthetized with pentobarbital sodium. The intracarotid sinus pressure (ISP) was altered in a stepwise manner in vivo. ISP-mean arterial pressure (MAP), ISP-Gain relationship curves and reflex characteristic parameters were constructed by fitting to the logistic function with five parameters. The changes in CBR performance induced by stress and the effects of microinjection with histaminergic receptors antagonists into the LC on the responses of CBR to stress were examined.</p><p><b>RESULTS</b>Stress significantly shifted the ISP-MAP relationship curve upwards (P < 0.05) and obviously moved the middle part of ISP-Gain relationship curve downwards (P < 0.05), and decreased the value of the MAP range and maximum gain (P < 0.05), but increased the threshold pressure, saturation pressure, set point and ISP at maximum gain (P < 0.05). Microinjection of selective H1 or H2 receptor antagonist, chlorpheniramine (CHL, 0.5 microg/microl) or cimetidine (CIM, 1.5 microg/microl) into the LC, significantly attenuated the above-mentioned changes in CBR performance induced by stress and the alleviate effect of CIM was less remarkable than that of CHL (P < 0.05). The responses of CBR under stress to H1 or H2 receptor antagonist generally occurred 20 min after the administration and lasted approximately for 16 min. Microinjection with the same dose of CHL or CIM into the LC in the unstressed group did not change CBR performance significantly (P > 0.05). However, microinjection of CHL or CIM into the LC could not completely abolish the stress-induced changes in CBR.</p><p><b>CONCLUSION</b>The stress results in a resetting of CBR and a decrease in reflex sensitivity. The stress-induced changes in CBR may be mediated, at least in part, by activating the brain histaminergic system. The H1 and H2 receptors in the LC, especially, Hi receptors may play an important role in the resetting of CBR under stress. The descending histaminergic pathway from the hypothalamus to LC may be involved in these effects. Moreover, the effects of stress on CBR also have other mechanisms.</p>

Circadian rhythms and different photoresponses of Clock gene transcription in the rat suprachiasmatic nucleus and pineal gland / 生理学报

The aim of this study was to observe and compare the endogenous circadian rhythm and photoresponse of Clock gene transcription in the suprachiasmatic nucleus (SCN) and pineal gland (PG) of rats. With free access to food and water in special darkrooms, Sprague-Dawley rats were housed under the light regime of constant darkness (DD) for 8 weeks (n=36) or 12 hour-light: 12 hour-dark cycle (LD) for 4 weeks (n=36), respectively. Then, their SCN and PG were dissected out every 4 h in a circadian day, 6 rats at each time (n=6). All animal treatments and sampling during the dark phases were conducted under red dim light (<0.1 lux). The total RNA was extracted from each sample and the semi-quantitative RT-PCR was used to determine the temporal mRNA changes of Clock gene in the SCN and PG at different circadian times (CT) or zeitgeber times (ZT). The grayness ratio of Clock/H3.3 bands was served as the relative estimation of Clock gene expression. The experimental data were analyzed by the Cosine method and the Clock Lab software to fit original results measured at 6 time points and to simulate a circadian rhythmic curve which was then examined for statistical difference by the amplitude F test. The main results are as follows: (1) The mRNA levels of Clock gene in the SCN under DD regime displayed the circadian oscillation (P<0.05). The endogenous rhythmic profiles of Clock gene transcription in the PG were similar to those in the SCN (P>0.05) throughout the day with the peak at the subjective night (CT15 in the SCN or CT18 in the PG) and the trough during the subjective day (CT3 in the SCN or CT6 in the PG). (2) Clock gene transcription in the SCN under LD cycle also showed the circadian oscillation (P<0.05), and the rhythmic profile was anti-phasic to that under DD condition (P<0.05). The amplitude and the mRNA level at the peak of Clock gene transcription in the SCN under LD were significantly increased compared with that under DD (P<0.05), while the value of corresponding rhythmic parameters in the PG under LD were remarkably decreased (P<0.05). (3) Under LD cycle, the circadian profiles of Clock gene transcription induced by light in the PG were quite different from those in the SCN (P<0.05). Their Clock transcription rhythms were anti-phasic, i.e., showing peaks at the light phase ZT10 in the SCN or at the dark time ZT17 in the PG and troughs during the dark time ZT22 in the SCN or during the light phase ZT5 in the PG. The findings of the present study indicate a synchronous endogenous nature of the Clock gene circadian transcriptions in the SCN and PG, and different roles of light regime in modulating the circadian transcriptions of Clock gene in these two central nuclei.