Effect of cerebral mild hypothermia on cerebral mitochondrial ATPase activity in neonatal rats with hypoxic-ischemic brain damage / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the effect of cerebral mild hypothermia on cerebral mitochondrial ATPase activities in neonatal rats with hypoxic-ischemic brain damage (HIBD).</p><p><b>METHODS</b>Eighty-four seven-day-old Wistar rats were randomly assigned into four groups: sham-operated normothermic, sham-operated mild hypothermic, HIBD normothermic and HIBD mild hypothemic. HIBD was induced by left common carotid artery ligation, followed by 8% hypoxia exposure. At each time interval of 2, 6, and 12 hrs post-hypoxia-ischemia (HI), 7 rats were sacrificed and the brain tissues were sampled for detecting the activities of mitochondrial Na+K+ATPase and Ca2+ATPase.</p><p><b>RESULTS</b>The activities of mitochondrial Ca2+ATPase decreased significantly in the two HIBD groups compared with those of the two sham-operated groups at 2, 6, and 12 hrs post-HI. The HIBD mild hypothemic group had higher mitochondrial Ca2+ATPase activities compared with the HIBD normothermic group at 2, 6, and 12 hrs post-HI (5.25 +/- 0.61 micromol/mgPr.h vs 3.17 +/- 0.81 micromol/mgPr.h 4.59 +/- 0.81 micromol/mgPr.h vs 2.26 +/- 0.53 micromol/mgPr.h4.61 +/- 0.62 micromol/mgPr.h vs 1.31 +/- 0.78 micromol/mgPr.H, respectively) (P < 0.01). The activities of mitochondrial Na+K+ATPase decreased significantly in the two HIBD groups compared with those of the two sham-operated groups at 6 and 12 hrs post-HI. A significant difference was observed in the mitochondrial Na+K+ATPase activities between the HIBD mild hypothemic and HIBD normothermic groups at 6 and 12 hrs post-HI (5.25 +/- 0.66 micromol/mg Pr.h vs 3.76 +/- 0.78 micromol/mgPr.h, 4.74 +/- 0.80 micromol/mgPr.h vs 3.12 +/- 0.53 micromol/mgPr.h; P < 0.01).</p><p><b>CONCLUSIONS</b>Mild hypothermia following HIBD inhibits the decline in cerebral mitochondrial Ca2+ and Na+K+ ATPase activities in neonatal rats, thus providing protective effects against HIBD.</p>

Mild hypothermia attenuates neuronal apoptosis after cerebral hypoxia-ischemia in neonatal rats / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the effects of mild hypothermia on sequential events of neuronal apoptosis following hypoxic-ischemic brain damage (HIBD) in neonatal rats.</p><p><b>METHODS</b>A model of HIBD was prepared by ligating the left common carotid artery in 7-day-old rats, followed by 8% hypoxia exposure. HIBD rats were randomly assigned into a hypothermia group (rectal temperature = 33 centi-degrees) and a normothermia group (rectal temperature = 36 centi-degrees). TUNEL, Haematoxylin and Eosin, and Nissl staining were used to detect neuronal apoptosis. Western blotting, RT-PCR and enzyme activity measurement were used to evaluate the changes of plasma and mitochondrial cytochrome c (Cyt c), caspase-3 mRNA expression and caspase-3 enzyme activity, respectively.</p><p><b>RESULTS</b>The number of apoptotic cells in the ipsilateral hemisphere of the hypothermia group was significantly reduced compared with that of the normothermia group at 72 hrs post-HI (6.4 +/- 1.7% vs 25.3 +/- 1.5%) (P < 0.01). Analysis of Western blotting showed that Cyt c levels increased in the cytosolic fraction, but decreased significantly in the mitochondrial fraction in the ipsilateral hemisphere of the hypothermia group at 24, 48 and 72 hrs of HI insult compared with the normothermia group (P < 0.05). Caspase-3 mRNA increased significantly after 24 hrs post-HI in the normothermia group, and this change became more pronounced with time. Mild hypothermia treatment decreased significantly caspase-3 mRNA expression at 24, 48 and 72 hrs post-HI (P < 0.05). Caspase-3 activity gradually increased 2 hrs after HI insult and peaked at 24 hrs in the normothermia group. Mild hypothermia treatment resulted in a significant reduction in caspase-3 activity in the ipsilateral hemisphere, with an optimal effect produced at 24 hrs post-HI (2.42 +/- 0.5 RFU vs 34.7 +/- 3.2 RFU; P < 0.01).</p><p><b>CONCLUSIONS</b>Mild hypothermia treatment attenuates neuronal apoptosis following HIBD, possibly through a reduction in Cyt c release from mitochondria and an inhibition of caspase-3 mRNA expression and its enzyme activity.</p>

Quantitative detection of intrahepatic hepatitis B virus DNA in patients with chronic hepatitis B / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To study the relationships between intrahepatic HBV DNA level and serum HBV DNA level, between intrahepatic HBV DNA level and hepatitis B e antigen (HBeAg) level in patients with chronic hepatitis B (CHB), and assess the valuation of pretreatment liver HBV DNA level in antivirus therapy.</p><p><b>METHODS</b>Liver specimens taken from 41 HBeAg-positive CHB patients before antivirus treatment were divided into two parts, one for histological examination, and the other for intrahepatic HBV DNA quantified detection by PCR-fluorescence. At the same time, serum levels of HBV DNA and HBeAg were detected. The patients were classified into two groups according to the pretreatment intrahepatic HBV DNA level (< or = 10(4)fg/cm(3) in group A, >10(4)fg/cm(3) in group B) and accepted interferon alpha-1b (3MU every day for 26 weeks) in combination with lamivudine (100mg per day for 52 weeks). During the treatment, the serum levels of alanine aminotransferase (ALT), HBV DNA and HBeAg seroconversion rate were monitored.</p><p><b>RESULTS</b>(1) The level of liver HBV DNA was much higher than that of serum HBV DNA (4.081 +/-1.127 vs 3.163 +/-1.010, t = 2.218, P < 0.05). Liver HBV DNA level had positive correlation to serum HBV DNA level (r = 0.840, t = 4.322, P < 0.001) and serum HBeAg level (r = 0.459, t = 3.056, P < 0.005). (2) Intrahepatic HBV DNA level was negative correlation to the severity of liver damage (chi(2) = 3.874, P < 0.05). (3) Serum HBV DNA level in all the patients reduced remarkedly after therapy, especially in group A. At the end of 52 weeks, the rates of HBeAg and anti-HBe seroconversion in group A were higher than those in group B (68.4% vs 36.4%, chi(2) = 4.194, P < 0.05; 73.7% vs 40.9%, chi(2) = 4.447, P<0.05).</p><p><b>CONCLUSIONS</b>Intrahepatic HBV DNA is a more valuable marker than serum HBV DNA or HBeAg to assess HBV replication, and can reflect the status of body immunity indirectly. It may be a useful indicator for the efficacy of antivirus treatment.</p>