Subarachnoid hemorrhage (SAH) elicits an inflammatory response in the subarachnoid space, which is mediated by the release of various cytokines. To assess their involvement in post-hemorrhagic complications, we determined the source and time-course of the release of inflammatory cytokines and acute-phase proteins in cerebrospinal fluid (CSF) following SAH. Concentrations of interleukin (IL)- 1beta, IL-6, transforming growth factor-beta1 (TGF-beta1) and C-reactive protein (CRP) in CSF of 36 patients with SAH were measured by enzyme-linked immunoabsorbent assay (ELISA). Floating cells collected from the CSF were centrifuged four to six days after SAH, and examined immunohistochemically. Intracellular IL-1beta and IL-6 were examined by flow cytometric analysis. The molecular weight of TGF-beta1 in CSF of 30 patients was examined by Western blot analysis. The TGF-beta1 levels of patients who had undergone ventriculoperitoneal (VP) shunt (n = 19) was significantly higher than nonshunt group (n = 16). The CRP levels of VP shunt group was significantly higher than nonshunt group. IL-6 concentration was maximal within day 0-1 and it was secreted by neutrophils and monocytes. ELISA showed consistently low levels of IL-1beta, whereas a proportion of monocytes and lymphcytes were IL- 1beta-positive by flow cytometric analysis. TGF-beta1 levels were also maximal on day 0-1 according to ELISA, although it tended to be in the inactive form derived from platelets. A 25 kDa band of TGF-1 was detectable for at least 13 days after SAH, which may have been secreted in part by neutrophils and monocytes. CRP levels in CSF peaked on day 2-3. The present results suggest that leukocytes induced by SAH play an important role in post-hemorrhagic inflammation in the subarachnoid space by releasing IL-6 and TGF-beta1. The CRP and TGF-beta1 levels in CSF are strongly concerned with communicating hydrocephalus after SAH.
The dura may serve as a strong barrier against tumour invasion into the intradural space, which emphasises the importance of not injuring the dura, when the tumour is removed extradurally. For radical removal of clival chordoma, it will be necessary to remove the tumour extensively including normal bone and soft tissues surrounding the tumour, especially the mucous membrane, because the normal mucous membrane is surgically difficult to preserve by dissecting it from the invaded submucous layer.
Nongerminomatous germ-cell tumor (NGGCT) in the central nervous system (CNS) is still highly lethal. The present study evaluated the outcome of high-dose chemotherapy followed by autologous stem-cell rescue (ASCR). The patients included three cases of choriocarcinoma, two cases of embryonal carcinoma and one case of yolk sac carcinoma. High-dose cisplatin (200 mg/m2), etoposide (1250 mg/m2) and ACNU (150 mg/m2) were administrated in combination with ASCR to patients at complete remission as a result of surgical removal, irradiation, and from four to seven courses of induction chemotherapy. All the patients treated with this therapy were alive from one to seven years after the diagnosis, living with good performance status. The patients have not required any additional treatments after ASCR. The myelosuppression period, characterized by fewer than 500/microl peripheral neutrophils, ranged from 8 to 15 days (median, 11.5 days). Within seven days of ASCR, high fever was found in four patients. Although mild liver dysfunction was found in all patients, renal dysfunction was not observed. Hearing disturbance was found in 50% of the patients. This treatment regime will improve long-term survival for patients with NGGCT.
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