Objective To explore the therapeutic effects of hyperbaric oxygen on neonatal hypoxic - ischemic encephalopathy (HIE) and its potential mechanism. Methods The serum neuron specific enolase (NSE) were tested by ELISA and plasma endothlin (ET) were detected with radio - immune - assay (RIA) before and after hyperbaric oxygen therapy. Results The serum NSE and plasma ET were (14. 72 ± 4. 26)μg/L and (76. 1 ± 19. 2) ng/L in the moderate group respectively and (15. 64 ± 5. 82) μg/L and (82. 5 ± 21. 6) ng/L in the severe group respectively. The NSE and ET were increased significantly in the moderate group and the severe group as compared with the control group (12. 47 ± 3. 49 μg/L,56. 32 ± 16. 7 ng/L respectively); The NSE and ET were (13. 58 ± 4. 57) μg/L and (62. 4 ± 18. 5) ng/L. in the mild group respectively and not increased significantly with the control group. The level of NSE and ET significantly decreased after hyperbaric oxygen was engaged. Conclusions The serum NSE and plasma ET were a good discriminator for the evaluation of HIE, and its dynamic changes might be one of the potential mechanisms for the therapeutic effects of hyperbaric oxygen on HIE.

Objective To study the changes of the plasma tumor necrosis factor - α (TNF - α) and calcitonin- gene related peptide (CGRP) levels and their clinical implication in neonates with hypoxic - ischemic encephalopathy (HIE). Methods Dynamic variations of plasma TNF - α and CGRP levels were measured in 38 neonates with HIE and 18 normal neonates by radioimmunoassay. Results Plasma TNF - α and CGRP levels increased markedly in the acute stage of HIE and were (1. 12 ± 0. 42) ng/ml and (88. 92 ± 23. 16 ) ng/ml respectively, especially in the severe group [ (1. 28 ± 0. 41) ng/ml, (118. 12 ± 30. 25)ng/ml respactively) ] and the moderate moderate group (0. 95 ± 0. 30) ng/ml, (86. 49 ± 24. 36)ng/ml respectively]. TNF-- α and CGRP levels which were (0. 61 ± 0, 18) ng/ml and (68. 39 1±19. 32) ng/ml with HIE were reduced to normal levee in the convalescence stage. There was a positive correlation correlation between plasma TNF - α and CGRP levels in the acute stage of HIE. Conclusions TNF- α and CGRP might be involved in the pathophysiologic process of HIE. TNF- α may yield scathing effects of cerebral injury in the acute statge. CGRP may play a protective role in HIE.

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Objective To study the detection of IgM antibodies against coxsackie B viruses and their significance of etiology and diagnosis for patients with myocarditis. Method seventy pediatric patients were divided into three groups: 20 cases of myocarditis, 25 cases of suspect myocarditis and 25 cases of the control group. The presence of CBV - IgM and CBV - IgG was detected by indirect ELISA. Results The test revealed 11 of 20 (55% ) CBV - IgM opitives in the myocarditis group, 11 of 25 (44% ) CBV- IgM positives in the indirect myocarditis group and 11 of 25 (44% ) CBVIgM positives in the control group. There were no significant differences among the three groups (x2 = 1. 1286, P > 0. 05). Conclusions The presence of CBV-IgM positive by indirect ELISA indicates that the patient is infected by CBV. It Is an etiologic evidence of patients with myocarditis. But it is not a clinical diagnostic evidence of patients with myocarditis.

Objective To evaluate the relationship between changes of cerebrospinal fluid (CSF) or blood S - 100 protein (S- 100), neuron specific enolase (NSE) levels and the severity of hypoxic - ischernic encephalopathy (HIE), and to explore the mechanism of changes of these protein levels. Method Seven - day postnatal SD rats were used. Their serial blood and CSF S - 100 and NSE were measured by radioimmunoassay. By using the RT - PCR technique the expression of mRNA for S - 100 and NSE in the brain tissue at different gluts of time after HI injury was tested. Immunohistochemical assay was used to investigate the changes of the expression of S - 100 and NSE at the protein level. Results The values of S - 100, NSE were (1. 205 ± 0. 183) μg/L and (3. 97 ± 0. 228) ηg/ml respectively at 24 hours and (1. 235 ± 0. 097) μg/L, (3. 76 ± 0. 234) ηg/ml respectively at 48 hours in the blood, were(1. 28 ± 0. 031 ) μg/L, (7. 15 ± 0. 717) ηg/ml respectively at 24 hours and (1. 32 ± 0. 097) μg/L, (4. 29 ± 0. 144)ηg/ml respectivaly at 48 hours in the CSF after HI injury. The values of S - 100, NSE were increased significantly in both the blood and CSF samples during 24-48 hrs after HI inujry than in the control group (0. 645 ± 0. 05 μg/L, 3. 15 ± 0. 164 ηg/ml and 0. 68 ± 0. 059 μg/L, 3. 42 ± 0. 322 ηg/ml respectively). The increment corresponded well with death cell counts in the brain after HI injury; a peak of rnRNA expression of NSE exnerged at 24 hours after HI injury, while S- 100 mRNA occurred at 48 hours. The positive area of the expression of S - 100 at the protein level increased progressively during 12-96 hrs, but the expression of NSE decreased significantly with the lapse of time. Conclusions S - 100 and NSE are senstitive markers for hypoxic-ischemic brain damage(HIBD). The appropriate time for sample collection is 24 - 48 hrs after HI injury. The mechanism of S - 100 level increase in the blood and CSF after HI injury is not only due to the leakage from damaged brain cells but also through a high expression Of S - 100 mRNA and S - 100 protein, while the elevation of NSE in the blood and CSF was mainly due to the leakage from neuronal damage.

Objective To explore changes of NF - κB and its inhibitory protein (IκB) in infection - induced cerebral edema, and to determine whether the protective effect of baicalin on infection - induced cerebral edema was related to the inhibitory effect on NF - κB activation and IκB degradation. Methods Forty - five healthy Sprague- Dawley (SD) rats were randomly assigned into three groups: the normal saline group (NS), the pertussis bacilli group (PB), and the baicalin - treated group (BC). In the BC group, baicalin was administered intraperitoneally every 4 hours from the first hour after the injection of pertussis bacilli. Electrophoretic mobility shift assay (EMSA) was performed on the nuclear extracts to detect the activity of NF - κB and Western blot analysis was performed to detect the expression of IκB - α. Results There was no significant NF- κB activation in the NS group. In the PB gruop, at 1-hour, the levels of NF- κB activation were similar to those in the NS group. In the PB group, at 2 hours, NF -κ B started to be activated. The activity of NF - κB reached the highest level in the PB group at 24 hours. The expression of IκBα began to decrease in the PB group at 2 hours and reached the lowerest level in the PB group at 24 hoars. There was no significant inhibitory effect on NF- κB activity and IκB - α degradation in the BC group at 1 hour. In the BC group, at 2 hours, 4 hours, 8 hours and 24 hours, the activities of NF - κB were lower than those in the relevant PB groups, and the expressions of IB were higher than those in the relevant PB groups. Conclusions NF - κB is strongly activated in infection-induced cerebral edema by pertussis bacilli. The elevation of NF - κB may be a key factor that induces brain edema. The protective effect of baicalin on infection - induced cerebral edema may be associated with the ichbitory effect on NF - κB, activation and IκB degradation.

Objective To observe the qualitative and quantitative alterations of laminins in glomerular diseases, and to clarify their biological and pathological significance to evaluate the role in the pathotgensis. Method Five laminin chains (α1, α2, β1, β2 and γ1 ) were studied by immunohisto - chemistry and in situ hybridization. The qualitative and quantitative changes of distribution and mRNA expression were observed in 48 renal biopsy specimens from patients with glomerular diseases. Results The mRNA expressions of α1, α2, β1 and γ1 increased with different degrees in glomeruli associated with mesangial proliferation. These increases originated from proliferative mesangial cells. Increased expressions of α1 and γ1 proteins and abnormal expressions of α1 and β1 proteins were found in the segments with mesangial proliferation and glomerulosclerosis, whereas the expression of β2 decreased in the mesangium and GBM of the same lesions in various degrees. Conclusions Proliferative mesangial cells are the origins of abnormal accumulation and expression of laminins in the measngial proliferative glomeruli. The quantitative and qualitative alterations of laminin chains distribution were found in glomerular diseases. It may be the basis of the progression and deterioration of glomerular diseases.

Objective To study the changes of TXB2 and 6 - keto - PGF1α in the, lung of immature rabbits with meconium aspiration. Methods We established mild and severe immature rabbit models of meconium aspiration by endotracheal intubation imbuing meconium 0. 6 ml/kg and 4 ml/kg. We measured the right ventricular pressure by right ventricular puncture. Levels of TXB2 and 6 - keto - PGF1α in the lung were measured by radioimmunoassay. Results In the mild group, the right ventricular pressure began to increase at 16 hours (2. 57 ± 0. 10 kPa), peaked at 24 hours (3. 57 ± 0. 14 kpa) and returned to the normal level by 72 hours (1. 89 ± 0. 04 kPa). The pressure of the severe group (4. 36 ± 0. 14 kpa)was significantly higher than that of the control (1. 85 ± 0. 05 kPa) and mild groups. Levels of TXB2 and 6 - keto - PGF1α. in the lung of the mild group increased significantly compared with the control group (76. 40 ± 16. 89 pg/ml; 56. 10 ± 16. 46 pg/ml), began to increase at 16 hours (153. 80 ± 15. 37 pg/ml, 117. 40 ± 22. 88 pg/ml),. peaked at 24 hours (369. 00 ± 28. 80 pg/ml; 207. 20 ± 28. 59 pg/ml) and recovered by 72 hours (103. 20 ± 11. 95 pg/ ml, 83. 62 ± 8. 76 pg/ml). The changes of the severe group (500. 60 ± 24. 58 pg/ml; 300. 00 ± 20. 31 pg/ml) were significantly different from those in the control and mild groups. The level of TXB2 and 6 - keto - PGF1. were correlated with the right ventricular pressure (r = 0. 95: 0. 96. P <0. 01). Conclusions TXB2 and 6 - keto -PGF1α in the lung significantly increase following the severity of meconium aspiration, indicating that TXB2 and 6 - keto - PGF1. influence the development of lung injury of meconium aspiration.