Spinal ventral roots of 10 infants were examined. Eight pairs of spinal ventral roots were cut off from 10 infant cadavers including the following segments: C_6, C_7,T_5, T_(11), L_3, L_5, S_1, and S_2. Serial longitudenal sections were prepared and stained with Niss's method. The presence of sensory neurons were recorded and their num- ber were counted. The results were as follows:Nerve cells in the spinal ventral roots were found in all the cases examined.The minimal number was 58 cells in No. 8, and the maximal number was 203 in No. 10. There were altogether 1,446 cells found in 117 spinal roots, and no cell in 35 roots. The highest number of nerve cells observed in a single root was 83.The nerve cells were scattered all over the spinal ventral root from its attachment to the spinal cord to its junction with the dorsal root. More cells were found in its distal extremity close to the spinal ganglion. They appeared singly, in groups of two or three, or in a cluster looking like a small ganglion. They were usually distributed among the nerve fibers, or around the blood vessels, or beneath the epineurium of the ventral root. They were ovoid in shape, with the long axis paralleling the course of nerve fibers. Nuclei were round in shape, Nissl granules were evenly distributed in the cytoplasm. They were different in sizes, ranging from 15 to 60 ?m. There were 808 cells (56%) more than 30～50 ?m. 607 cells (42%) less than 30 ?m, which accounted 98% of the total cell population.

Objective: To explore the effect of trimetazidine (TMZ) on T-peak (Tp) to T-end (Te) interval of resting ECG in patients with unstable angina pectoris (UAP) after percutaneous coronary intervention (PCI). Methods: We investigated 94 UAP patients with PCI and 76 of them ifnished the study as 2 groups. Control group,n=42, the patients received conventional treatment, and TMZ group,n=34, in addition to conventional treatment, the patients received TMZ 60 mg at 0.5 to 1 hour before PCI. The changes of Tp to Te interval before and after PCI were calculated, serum levels of creatine kinase (CK), creatine kinase-MB (CK-MB) and cardiac troponin I (cTnI) at before and at 6, 24 hours after PCI were compared between 2 groups. Ventricular arrhythmia was recorded during PCI. Results: Both groups had shortened Tp to Te intervals after PCI, and TMZ group had more shortened Tp to Te interval, bothP<0.05, while the Tp to Te intervals were similar between 2 group before PCI,P>0.05. The occurrence rate of ventricular arrhythmia in Control group was higher than that in TMZ group (12.52% vs 5.16%) during PCI,P<0.05. Compared with Control group, TMZ group had lower levels of CK, CK-MB and cTnI at 6, 24 hours after PCI, allP<0.05. Conclusion: TMZ could decrease Tp to Te interval of resting ECG, prevent ventricular arrhythmia and reduce the relevant myocardial injury in UAP patients after PCI.

Objective To investigate the echocardiographic features in patients with right atrial myxoma and thus evaluate the value of echocardiog?raphy in the diagnosis of right atrial myxoma. Methods The echocardiographic findings of 20 patients with right atrial myxomas were retrospectively analyzed,and the echocardiographic features of these patients were summarized. Results The main clinical symptoms of right atrial myxoma includ?ed chest tightness,shortness of breath,lower limb edema,and syncope. Of these 20 patients,the echocardiography showed that the average size of the right atrial myxomas was 3.11 cm × 2.90 cm to 7.44 cm × 4.52 cm. The myxomas were round or oval shape in 15 patients(75%)and lobulated shape in 5(25%). The myxomas were attached to the atrial septum in 15 patients(75%)and to right atrial free wall in 25%of the patients. The aver?age width of the basement was 1.62±0.30 cm,and the width was greater than 1 cm in 80%of the patients had the width over 1 cm. Some myxomas had internal areas of calcification and anechoic cystic areas. The percentages of patients with the blocking of right atrium,tricuspid and pulmonary hy?pertension were 70%,50%,and 10%,respectively. Conclusion The echocardiographic features of right atrial myxoma were specific. Echocardiog?raphy can accurately assess the tumor and identify the secondary changes in cardiac structure and hemodynamics and thus provide evidence for time?ly and accurate diagnosis of right atrial myxoma.

Objective To explore the protective effect of pre-operation administration of nicorandil on myocardial injury and recurrent angina in patients with unstable angina pectoris who underwent percutaneous coronary intervention (PCI). Methods A total of 91 patients with unstable angina pectoris were admitted for PCI and randomly divided into 2 groups who either received nicorandil(5 mg tid)or not for 7 days prior to the procedure and routine dose of nicorandil (5mg tid) after it. The concentrations of creatine kinase MB (CK-MB) and cardiac troponin I(cTnI) were compared between two groups before PCI and 6 hours, 18 hours and 24 hours after PCI;Recurent angina and major adverse cardiac events,includ-ing death,re-infarction and stroke at 6 months after the procedure were also chased and compared. Results In total, 75 pa-tients who were successfully undergone elective PC1 were finally enrolled,among whom 37 cases were in nicorandil group and 38 cases were in routine group. Post-procedural levels of CK-MB and cTnI significantly reduced in the nicorandil group between 6~24 h (P<0.05) compared those in routine group.At 6 months follow-up,symptoms of recurrent angina after PCI were significantly relieved in the nicorandil group compared with that in routine group (P < 0.05).Conclusion nicorandil can limit the PCI-induced myocardial injury and relieve the symptoms of recurrent angina after PCI in patients with unstable angina.

Objective To observe the change of Toxoplasma g ondii tachyziote in pseudocyst. Methods The mice infected by RH Toxoplasma were treated with mandelic acid (200 mg?kg -1 , twice daily) orally or intravenously, then ascites was taken out to smear in 24 h, 72 h and the time of death, with Giemsa dye and transmission electronic microscope (TEM), the survival time was c alculated. Results Under the light microscope, the cell mem brane of tachyzoite was tortous and broken, the bubble and pelletish material we re observed in cytoplasm, cell nucleus was split; but the cell membrane, organs and nucleus were destroyed more obviously under the TEM than those under the lig ht microscope. Meanwhile the living time of mice treated by mandelic acid (8.0 d ays in oral administration group and 6.8 days in intravenous administration grou p) was obviously longer than that in positive control group(5.5 days, P

Objective To evaluate the effects of ulinastatin preconditioning on protamine-induced pulmonary injury in patients undergoing cardiac valve replacement under cardiopulmonary bypass (CPB).Methods Sixty NYHA class Ⅱ or Ⅲ and ASA physical status Ⅱ or Ⅲ patients of sexes,aged 21-59 yr,scheduled for elective cardiac valve replacement under CPB,were randomly divided into 3 groups (n =20 each):group control one protamine given via central vein (group C1) ; group control two protamine given via ascending aorta (group C2) ;group ulinastatin preconditioning (group U).Heparin was neutralized with protamine after termination of CPB.Ulinastatin 20 000 U/kg was infused via the central vein at a rate of 500-1000 U· kg-1 · min-1 starting from the time point after tracheal intubation until 10 min before cross-clamping of superior vena cava and inferior vena cava in group U.At 10 min after termination of CPB,protamine 4 mg/kg was infused over 8 min via the right internal jugular vein in groups C1 and U,or via the aortic root in group C2.Blood samples were obtained from the left atrium and right atrium at 5 min before neutralization of heparin with protamine (T1) and 15 min after neutralization of heparin with protamine (T2) for determination of polymorphonuclear leukocyte (PMN) and platelet (Plt) counts,and plasma concentrations of thromboxane B2 (TXB2) and 6-keto-prostaglandin F1α (6-keto-PGF1α).Blood samples were obtained from the left atrium at T1 and T2 for determination of the levels of TNF-α,IL-1,IL-8,CD11b/CD18,C3a,C5a,and malondialdehyde (MDA) and superoxide dismutase (SOD) activity and for blood gas analysis.Alveolar-arterial oxygen gradiant (A-aDO2),respiratory index (RI) and oxygenation index (OI) were calculated.Pulmonary arterial pressure (PAP) was recorded.Results Plt and PMN counts in the blood obtained from the left atrium were significantly lower,and plasma TXB2 concentrations in the blood obtained from the left atrium were higher at T2 in group C1,and the plasma 6-keto-PGF1α concentrations and SOD activity in the blood obtained from the left atrium were higher at T2 in groups C2 and U than those in the blood obtained from the right atrium (P ＜0.05).Compared with group C1,Plt and PMN counts and plasma 6-keto-PGF1α concentrations were significantly increased,the levels of plasma TXB2,TXB2/6-keto-PGF1α,TNF-α,IL-1,IL-8,C3a,C5a and MDA were decreased,CD11b/CD18 expression was down-regulated,PAP,A-aDO2 and RI were decreased,and OI was increased at T2 in C2 and U groups (P ＜ 0.05).There were no significant differences in the parameters mentioned above between groups C2 and U (P ＞ 0.05).Conclusion Ulinastatin preconditioning can inhibit protamine-induced pulmonary injury in patients undergoing cardiac valve replacement under CPB,and the effect is similar to that of protamine administered via the aorta.

Objective To investigate the role of phosphatidylinositol 3-kinase (PI3K)/protein-serine-threonine kinases (Akt) signal pathway in ulinastatin postconditioning-induced attenuation of apoptosis in myocardial cells in patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Forty NYHA class and ASA physical status Ⅱ or Ⅲ patients of both sexes,aged 21-59 yr,scheduled for cardiac valve replacement with CPB,were randomly divided into 2 groups (n =20 each):normal saline control group (group C) and ulinastatin postconditioning group (group U).In group U,ulinastatin 10 000 U/kg was perfused via the aortic root at 4000-5000 U· kg-1 · min-1 starting from 5 min before aortic unclamping.In group C,the equal volume of normal saline was given instead of ulinastatin.Myocardial specimens were taken from the right auricle at 45 min after aortic unclamping for determination of the expression of Akt,phosphorylated Akt (p-Akt),cytochrome c,caspase-9,Bcl-2 and Bax,and cell apoptosis.Bcl-2/Bax ratio and apoptotic index were calculated.Results The expression of p-Akt and Bcl-2 and Bcl-2/Bax ratio were significantly higher,and the expression of cytochrome c,caspase-9 and Bax and apoptotic index were lower in group U than in group C (P ＜ 0.05).Conclusion Ulinastatin postconditioning attenuates apoptosis in myocardial cells in patients undergoing cardiac valve replacement with CPB through activating PI3K/Akt signal pathway.

Objective To evaluate the effects of ulinastatin on renal ischemia-reperfusion injury in patients undergoing operation on aorta with deep hypothermic circulatory arrest (DHCA ) .Methods Thirty patients ,aged 30-50 yr ,of ASA physical status Ⅲ or Ⅳ (NYHA Ⅱ or Ⅲ) ,scheduled for elective operation on aorta with DHCA ,were randomly divided into 2 groups ( n=15 each) using a random number table :control group (group C ) and ulinastatin group (group U ) .In group U ,ulinastatin 20 000 U/kg was infused via the central vein at 500-1 000 U·kg-1 ·min-1 from the time immediately after tracheal intubation until 10 min before ascending aortic cross-clamping .In group C ,the equal volume of normal saline was infused instead of ulinastatin .At 5 min before the beginning of DHCA (T1 ) and 15 min after the end of DHCA (T2 ) ,blood samples were taken from the extracorporeal circulation for determination of polymorphonuclear leukocyte counts , and plasma levels of intercellular adhesion molecule-1 , tumor necrosis factor-α, iterleukin-6 (IL-6 ) IL-8 , IL-10 , malondialdehyde , myeloperoxidase ,atrial natriuretic peptide ,cystatin C ,and creatinine .Results The polymorphonuclear leukocyte counts and plasma levels of intercellular adhesion molecule-1 , tumor necrosis factor-α, IL-6 , IL-8 , malondialdehyde , myeloperoxidase , cystatin C , and creatinine were significantly lower , and the plasma concentrations of IL-10 and atrial natriuretic peptide were higher in group U than in group C ( P< 0.05 ) . Conclusion Ulinastatin can attenuate renal ischemia-reperfusion injury in patients undergoing operation on aorta with DHCA and inhibition of inflammatory responses is involved in the mechanism .

Objective To evaluate the role of Fas/FasL signaling pathway in ulinastatin postconditioning-induced attenuation of apoptosis in the myocardial cells of patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Forty patients of both sexes,aged 21-59 yr,of ASA physical status Ⅱ or Ⅲ (NYHA class Ⅱ or Ⅲ),scheduled for elective cardiac valve replacement with CPB,were randomly divided into 2 groups (n =20 each):control group (group C),and ulinastatin postconditioning group (group U).In group U,ulinastatin 10 000 U/kg was perfused via the aortic root at 4 000-5 000 U·kg-1 ·min-1 starting from 5 min before aortic unclamping.In group C,the equal volume of normal saline was infused instead of ulinastatin.Myocardial specimens were taken from the right auricle at 45 min after aortic unclamping for determination of Fas,Fas ligand (FasL),caspase-8,Bcl-2 and Bax expression and cell apoptosis.The ratio of Bcl-2 expression to/Bax expression (Bcl-2/Bax) and apoptotic index were calculated.Results Fas,FasL,caspase-8 and Bax expression and apoptotic index were significantly lower,and Bcl-2 expression and Bcl-2/Bax were higher in group U than in group C.Conclusion Ulinastatin postconditioning attenuates apoptosis in the myocardial cells through inhibiting Fas/FasL signaling pathway in the patients undergoing cardiac valve replacement with CPB.

Objective To evaluate the effects of ulinastatin postconditioning and combination of ulinastatin preconditioning and postconditioning on myocardial apoptosis in patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Eighty New York Heart Association (NYHA) class Ⅱ or Ⅲ patients of both sexes,aged 21-59 years,scheduled for cardiac valve replacement with CPB,were randomly divided into four groups (n =20 each):normal saline control group (group C),ulinastatin preconditioning group (group U1),ulinastatin postconditioning group (group U2) and ulinastatin preconditioning plus postconditioning group (group U3).In group U1,uinastatin 20000 U/kg was infused via the central vein at 500-1000 U·kg-1 · min-1 after endotracheal intubation until 10 minutes before blocking the ascending aorta.In group U2,ulinastatin 10000 U/kg was infused via the aortic root at 4000-5000 U· kg-1 · min-1 at 5-7 minutes before opening the aorta.In group U3,ulinastatin preconditioning and postconditioning were performed as described in groups U1 and U2.In group C,the same volume of normal saline was infused instead of ulinastatin.Blood samples were taken from the radial artery at 10 minutes before blocking the ascending aorta,40 minutes after blocking the ascending aorta,45 minutes after opening the aorta and at the end of operation for determination of plasma concentrations of tumor necrosis factor-alpha (TNF-α) and soluble tumor necrosis factor receptor 1 (sTNF-R1).Myocardial tissues were obtained from the right atrial appendage at 45 minutes after opening the aorta for determination of the expression of TNF-α,bcl-2,bax,caspase-3,and apoptosis.The bcl-2/bax ratio and apoptotic index were calculated.Results Plasma concentrations of TNF-α and sTNF-R1 and the expression of TNF-α,bax,caspase-3 and apoptotic index were lower and the expression of bcl-2 and bcl-2/bax ratio were higher in groups U1,U2 and U3 than in group C and they were lower in group U3 than in groups U1 and U2 (P ＜ 0.05).Conclusion Ulinastatin postconditioning can inhibit myocardial apoptosis in patients undergoing cardiac valve replacement with CPB,and the efficacy of combination of ulinastatin preconditioning and postconditioning is stronger than that of ulinastatin postconditioning.The mechanism is involved in balancing the expression of bax and bcl-2 and down-regulating the expression of TNF-α and its receptor.