ABSTRACT
Objective To investigate the secondary degeneration of corticospinal tracts in cervical spinal cord following a recently cerebral infarct with diffusion tensor imaging(DTI) and its potential impact on neurological recovery.Methods Twenty-six patients with a focal cerebral infract underwent DTI at the first week, the fourth and twelfth week after stroke onset, respectively.The NIH Stroke Scale (NIHSS), the Fugl-Meyer motor scale (FM) and the barthel index (BI) were used to evaluate the neurological function before every DTI.Twenty-six gender and age match healthy volunteers underwent DTI three times at same time points.The DTI parameters of mean diffusivity (MD) and fractional anisotropy (FA value) were measured at the cervical spinal cord and initial lesion.Results Compared to the controls, the FA values of the contralateral side corticospinal tracts in the cervical spinal cord in patients significantly decreased at every observed time point (P<0.01).In patients group, the FA values of the contralateral side corticospinal tracts in the cervical spinal cord decreased progressively from 1~(st) week to 12~(th) week (P<0.01), but MD remained unchange.The absolute value of the percent reduction of FA value of the contralateral side corticospinal tracts in the cervical spinal cord in patients associated negatively with the absolute value of the percent change of NIHSS and FM (P<0.05), but not with the absolute value of the percent change of BI(P>0.05).Conclusions Conclusions: The secondary degeneration of the corticospinal tracts resulted from cerebral infarction may extend to the cervical spinal cord.Which may last at lest three months and thus hamper the process of neurological recovery.
ABSTRACT
Objective: To construct severe acute respiratory syndrome (SARS)coronavirus 3CL protease gene into transforming vector prepare recombinant baculovirus and transduct it into infect insect cells to express SARS-3CL protease. Mothods: The 3cl-Teasy and pFastBac HTb bacmida were amplified. The 3cl gene was cloned into baculovirus transforming vector pFastBac HTb by enzyme-digest- and-ligase method,which was named recombinant pFB HTb-3cl. The pFB HTB-3cl was transformed into E.coli DH10Bac competent cells.The positive colonies were screened by three antibiotics and blue-white patch method. The bacmid-HTb-3cl recombinant baculovirus bacmid was obtained and purified to transfect St9 insect cells.The protease expressed in Sf9 insect cells were identified by SDS-PAGE. Results: Recombinant expression vector was obtained successfully. The 3CL protease expressed in insect cells were identified by SDS-PAGE. Conclusion: The expression of 3CL protease in insect cells provided foundation for detecting protein activities and screening inhibitor against SARS-3CL protease.
ABSTRACT
Objective To investigate whether delayed treatment with exogenous kallikrein on neurogenesis after focal cortical infarction in stroke-prone renovascular hypertensive rats (RHRSP). Methods Seventy-two RHRSP were divided into 3 groups. Twenty-four rats were given human tissue kallikrein ( 1.6 × 10-2 PNAU/kg) and 24 rats were given vehicle through tail venous daily for 2 or 6 days consecutively starting at the 24th hour after distal middle cerebral artery occlusion (MCAO). 24 rats underwent sham-operation. Cell proliferation was examined by using 5'-bromo-2'-deoxyuridine (BrdU, 50 mg/kg). Rats were respectively sacrificed 3, 7, 14 or 28 days after MCAO. Results Treatment with kallikrein significantly increased the number of BrdU+ cells in the ipsilateral subventricular zone (SVZ) (304.0±73. 9 vs 167.0±32.2 vs 56.0±12.2 at 7 d after operation, q =7.165, 12.916 and 5.751 respectively,all P<0.05) and in the peri-infarction region (490.0±82.0 vs 308.0±51.5 vs 49.0± 9.5 at 7 d after operation, q = 7.920, 19.184 and 11.264 respectively, all P < 0.01 ), and increased the number of BrdU+/DCX+ cells (225.0±13.6 vs 98.0±9.6 vs 23.0±5.6 at 7 d after operation, q = 30.731,48.735 and 18.004 respectively,all P < 0.01) in the ipsilateral SVZ compared with the vehicle group or the sham-operated group, which began on the 3 day, peaked in 7--14 days after MCAO, and then gradually decreased. Compared with the vehicle group, exogenous kallikrein markedly increased the number of BrdU+/NeuN+ cells (21.0±3.4 vs 13.0±2.6 at 14 d, P =0.001 ) in the peri-infarction region after MCAO. The kallikrein group showed a better functional improvement than the vehicle group after stroke ( all P < 0.05). Conclusion Our study suggests that administration of exogenous kallikrein at 24 h after cortical infarction enhances the SVZ neuroblasts proliferation, migration, and selective differentiation and improves functional recovery after stroke.