The clinical use of fetal neural grafts as an intracerebral source of dopamine for patients with Parkinson's disease has met with limited success. Since basic fibroblast growth factor (bFGF) enhances the survival and growth of dopaminergic neurons in vitro, we explored whether cells genetically modified to produce bFGF would improve the functional efficacy of dopaminergic neurons implanted into rats with experimental Parkinson's disease. Results show that bFGF-producing cells grafted together with fetal dopamine neurons have potent growth-promoting effects on the implanted neurons in vivo. Moreover, rats implanted with such co-grafts display the most pronounced behavioural improvements post-grafting. These findings not only provide insight into the function of bFGF in situ, but also suggest an approach for enhancing the survival and function of dopamine neurons grafted into the damaged brain.

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A 21-year-old man with double intracranial tumours of maldevelopmental origin, teratoma at the pineal region and an epidermoid cyst in the fourth ventricle, is reported. The tumours were removed totally by multiple operations; the epidermoid cyst was resected by suboccipital craniectomy with the patient in prone position and the teratoma was removed via occipital transtentorial approach with the patient in sitting position. Maldevelopmental tumours located within the cranial cavity with different histological types such as the present case have not sofar been described. Histogenesis of these tumours is confusing because teratoma often contains tissues of epidermoid cyst. Etiological considerations for these tumours are presented and appropriate operative procedures for tumours simultaneously occurring in the pineal and the fourth ventricle are also discussed.

Basic fibroblast growth factor (FGF‐2) is normally expressed as a cell‐associated protein, and accordingly it is not clear how it exerts its action on target cells in vivo. It has been proposed that cells release, by death or other mechanisms, small amounts of FGF‐2 that then acts in an autocrine manner. To address the question of whether it is necessary that FGF‐2 remain cell associated or needs to be secreted from cells to have biological activity, we expressed the 18‐kDa form of FGF‐2 in primary fibroblasts as a cell‐associated (FGF‐2‐B) or as a secreted (FGF‐2‐S) protein. FGF‐2 protein is detected in cell lysates and membrane fractions of both cell types, whereas it is present in significant amounts only in the conditioned medium of FGF‐2‐S cells. No FGF‐2 is detected in control (untransfected) cells. FGF‐2‐S cells also grow faster than the control or FGF‐2‐B cells. Yet, when evaluated for their ability to promote the survival of embryonic hippocampal neurons in vitro, both the cell types are active, establishing the activity of the transgene product. We conclude that FGF‐2 is active when engineered to be expressed as a cell‐associated form or secreted from cells.

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Dissociated cells prepared from the cerebellar primordia of normal 15-day mouse embryos were grafted into the cerebellum of 1-month-old weaver mutant mice which are characterized by degeneration of cerebellar granule cells during the early postnatal period. The growth of the grafted cells was investigated at 1 month after the operation. Implanted cells were highly developed to form a large mass of tissue in the host cerebellar folia. Histological examination revealed that a trilaminar cortical structure was partially developed in certain areas of the grafted tissue. The implanted granule-like cells were labeled with [3H]thymidine which was injected into the host, suggesting that the granule-like cells actively proliferate in the host cerebellum after the transplantation. In this area, strong immunoreactivity with synapsin I was detected indicating that the dissociated granule cells of the cerebellar primordia are able to develop a synaptic organization in the weaver mouse cerebellum.

A nonfamilial case of Turcot syndrome (glioma-polyposis syndrome) is described. A 16-year-old male with no siblings first developed a frontal astrocytoma, and was later found to have colonic polyposis with adenocarcinoma. The family history was negative for the syndrome, but his parents were first cousins.

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