| Project/Area Number |
06807111
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Cerebral neurosurgery
|
|---|
| Research Institution | SHINSHU UNIVERSITY |
|---|
Principal Investigator |
TADA Tsuyoshi SHINSHU UNIV., SCHOOL OF MEDICINE,LECTURER, 医学部・脳神経外科, 講師 (00236530)
|
|---|
| Project Period (FY) |
1994 – 1995
|
| Project Status |
Completed (Fiscal Year 1995)
|
| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1995: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1994: ¥1,600,000 (Direct Cost: ¥1,600,000)
|
|---|
| Keywords | communicating hydrocephalus / TGF-beta1 / subarachnoid hemorrhage / cerebrospinal fluid / normmal pressure hydrocephalus / C57 / BL6 / TGF-β1 / 水頭症 / TGF-β / クモ膜下出血 |
|---|
| Research Abstract |
We injected human recombinant TGF-beta1 into the subarachnoid space of 10-day-old C57BL/6 mice in order to study the role of TGF-beta1, which is known to be released from platelets into the cerebrospinal fluid following subarachnoid hemorrhage(SAH). The ventricular system became dilated within 3 weeks following the injection and the body weights of injected mice stopped increasing 6 weeks after injection of TGF-beta1. Microscopic examination revealed dilatation of the ventricular system, and that the outlets of the ventricles were not obliterated.Electron microscopy showed diminution of cilia on the ependyma. These results demonstrate that TGF-beta1 induces communicating hydrocephalus in mice. To examine the role of TGF-beta1 in similar condition of SAH,we injected autologous serum or plasma in the subarachnoid space. The results showed that the hydrocephalus could be induced by serum not by plasma, and the generation was blocked by human anti-TGF-beta1 antibody.
The aim of next study w
… More
as to determine whether TGF-beta1 is related to the development of communicating hydrocephalus after SAH.TGF-beta1 in the cerebrospinal fluid of 24 patients with SAH was measured with ELISA system. The levels were compared between hydrocephalic and non-hydrocephalic groups. Western blot analysis was performed to determine active TGF-beta1 in the cerebrospinal fluid. TGF-beta1 rapidly decreased from the onset of SAH.TGF-beta1 of 13 cases showing ventricular dilatation with periventricular low density on CT scan was 1.07(]SY.+-。[)0.37ng/ml at day 12-14, which was significantly higher than 0.52(]SY.+-。[)0.21ng/ml of cases without ventricular dilatation(p<0.01). Furthermore, TGF-beta1 of cases that had undergone ventriculo-peritoneal shunt(n=11)was 1.11(]SY.+-。[)0.09ng/ml at day 12-14, which was also higher than 0.56(]SY.+-。[)0.22ng/ml of the non-shunt group(n=13)(p<0.01). A 25 kDa band was demonstrated by western blot analysis in the cerebrospinal fluid of a patient with SAH.Our results strongly suggest that TGF-beta1 plays an important role in generating communicating hydrocephalus following SAH. Less
|
