Objective:To study the activity of immunological regulative function of red blood cells of the patients with chronic renal failure.Methods:The proliferative reaction of the erythrocyte promoting lymphocyte was detected in CRF patients and healthy persons with MTT colorimetry,in which the normal person's lymphocyte as the target cell and the erythrocyte as the stimulating cell.Results:It was found that the healthy persons of control group had obvious proliferative reaction of the erythrocyte promoting lymphocyte(promoting rate:57.3%?10.2%),while the 36 CRF patients had lower proliferative activity(promoting rate:32.7%?7.8%,P

Objective To explore the application of diffusion tensor imaging (DTI)in crossed cerebellar diaschisis (CCD)of cerebral gliomas. Methods MR images of 17 patients with high grade gliomas and 20 patients with low grade gliomas confirmed by postoperative pathology and 18 normal controls were analyzed retrospectively.The fractional anisotropy (FA)of cerebellar hemisphere was quantitatively measured with DTI technique.The asymmetry index (AI)of cerebellar hemispheric was calculated and compared in patients.The correlation between CCD phenomenon and histological grade of cerebral gliomas was also analyzed.Results Compared with ipsilateral cerebellar hemisphere of cerebral high grade gliomas,the FA value of contralateral cerebellar hemisphere significantly reduced (t=3.42,P<0.05).But there were no significant differences of FA values between contralateral cerebellar hemisphere and ipsilateral cerebellar hemisphere in cerebral low grade gliomas patients (t=0.80,P>0.05).The AI values of cerebellar hemisphere in high grade gliomas increased compared with low grade gliomas and normal controls (t=4.15,P<0.05;t=4.68,P<0.05),but there were no significant differences in the AI values of cerebellar hemisphere between low grade gliomas patients and normal controls (t=0.79,P>0.05).Conclusion CCD phenomenon is associated with the histological grade of cerebral gliomas.High grade gliomas can cause CCD phenomenon,but there is no evident CCD phenomenon in low grade gliomas.DTI technique is able to quantitatively assess CCD noninvasively by FA parameter.

Objective To investigate whether mild hypothermia can promote neurogenesis in the dentate gyrus of hippocampus and cognitive function recovery after traumatic brain injury ( TBI) through inhibiting apoptosis of hippocampal neurons. Methods A total of 66 healthy adult Sprague-Dawley rats were randomly divided into sham group, TBI group and TBI+hypothermia group, with 22 rats in each group. The rat TBI model was established using the fluid percussion device. The rats in TBI +hypothermia group received 4-hour hypothermia therapy immediately after injury, with the target temperature of 33. 5℃. Bromodeoxyuridine (BrdU) was injected into the rats' abdominal cavity to label the mitotic cells. The test of Morris water maze was used to evaluate the rats' spatial learning and memory capabilities. Immunofluorescence staining was used to observe the expression levels of BrdU, doublecortin (DCX), neuron specific nuclear protein (NeuN), cysteinyl aspartate specific proteinase 3 (caspase-3) and cleaved caspase-3 expressions in dentate gyrus of hippocampus at 7 days and 28 days after injury. Expressions apoptosis-related proteins including the factor associated suicide ( FAS )/factor associated suicide ligand (FASL), B-cell lymphoma-2 (Bcl-2), caspase-3 and cleaved caspase-3 expressions were detected by Western blot assay. Results The water maze tests at 28 days after injury showed that compared with TBI group, the escape latency in TBI+hypothermia group was significantly shorter [(24. 2 ± 5. 9)s:(18 ± 4. 1)s], and both the time in the target quadrant and the number of platform crossing were increasedsignificantly[(24.9±6.5)s:(31.7±5.2)s; (1.9±0.8) times:(3.5±1.2)times](P<0. 05). Compared with the sham group, in TBI group and TBI+hypothermia group, the BrdU+ new-born cells in the dentate gyrus of hippocampus were significantly increased at 7 days after injury [(9. 4 ± 4. 1):(33. 4 ± 3. 8);(9. 4 ± 4. 1):(45. 8 ± 5. 6)], the BrdU+ /DCX+ new-born neurons were increased at 7 days after injury [(2. 0 ± 0. 6):(9. 6 ± 1. 6);(2. 0 ± 0. 6):(19. 2 ± 3. 7)], and the BrdU+ /NeuN+mature neurons were increased at 28 days after injury [(2. 6 ± 1. 0) :(17. 2 ± 3. 9); (2. 6 ± 1. 0) :(33. 6 ± 9. 1)] (P<0. 01). TBI group showed more obvious increase than the TBI+hypothermia group (P<0. 01). Moreover, compared with 7 days after injury, the number of BrdU+ cells at 28 days after injury was further increased in TBI +hypothermia group but decreased in TBI group [(45. 8 ± 5. 6) :(58. 8 ± 9. 2);(33. 4 ± 3. 8):(22. 0 ± 3. 5)](P<0. 05 or <0. 01). Compared with the sham group, the caspase-3 +NeuN+ and caspase-3 +NeuN+ apoptotic neurons were significantly increased at 7 days after injury in TBI group [(2. 0 ± 0. 9):(11. 6 ± 2. 6); (2. 6 ± 1. 0):(10. 2 ± 2. 9)] (P<0. 05). Compared with the TBI group, the cleaved caspase-3 +NeuN+ apoptotic neurons were decreased in TBI+hypothermia group [(6. 6 ± 2. 0):(11. 6 ± 2. 6)](P<0. 05). Furthermore, compared with the TBI group, mild hypothermia might down-regulate the expression of FAS, FASL, cleaved caspase-3 and caspase-3 and up-regulate the expression of Bcl-2 in the hippocampus [(1. 54 ± 0. 15) :(1. 14 ± 0. 12);(1. 06 ± 0. 04):(0. 80 ± 0. 09); (0. 84 ± 0. 03):(0. 62 ± 0. 08); (0. 93 ± 0. 06):(0. 86 ± 0. 09);(0. 71 ± 0. 01):(1. 58 ± 0. 18)](P<0. 05). Conclusions Mild hypothermia might inhibit apoptosis of hippocampal neurons through cleaved caspase-3, FAS/FASL and Bcl-2 pathways, thus improving the neurogenesis and maturation of neurons in the dentate gyrus of hippocampus and facilitating cognitive function recovery in rats. It indicates that the function of hypothermia in anti-apoptosis and neurogenesis and maturity of hippocampal neurons may have a potential role in predicting the prognosis of TBI patients.