Taurine is involved in cell volume homeostasis, antioxidant defense, protein stabilization, and stress responses. High levels of intracellular taurine are maintained by a Na+-dependent taurine transporter (TAUT) in the plasma membrane. In view of the immunomodulatory and cytoprotective effects of taurine, a mouse model with a disrupted gene coding for the taurine transporter (taut-/- mice) was generated. These mice show markedly decreased taurine levels in a variety of tissues, a reduced fertility, and loss of vision due to severe retinal degeneration. In particular, the retinal involvement identifies the taurine transporter as an important factor for the development and maintenance of normal retinal functions and morphology.

The proposed method is easy to apply in clinical routine MR investigations and provides valuable information for noninvasive, preoperative assessment of tumor grading. It can also provide additional criteria for estimating the histological outcome and with it the degree of ischemia in stroke patients.

Neither sevoflurane nor ischaemic preconditioning preserves renal function or attenuates cell damage in the rat in vivo.

Cell differentiation is not seriously affected by the lack of a functional taurine transporter but mature photoreceptor cells do not survive without an intact transporter, even in the dark.

Desflurane post-conditioning protects renal function and tissue. This protection was greater after the short episode than after the long episode of ischaemia.

A hydrocephalic-hydromyelic condition was induced in adult cats by causing the closure of the lateral apertures with intracisternal injections of kaolin. After displaying the symptoms characteristic of increased intracranial pressure, which lasted about 10-14 days but varied somewhat in intensity from animal to animal, the cats recovered. From approximately the 2nd post-operative week onward, a distended central canal was revealed by ventriculography; subsequently cavities developed in the tissue of the cord that communicated with the canal. Most cavities were located dorsal to the canal. The surfaces of the distended canal and the cavities showed that in ventral areas the ependyma streched but remained intact, whereas in dorsal areas it ruptured, exposing the nerve fibers to the cerebrospinal fluid (CSF). In cats which had been hydrocephalic for up to 2 years the walls of the cavities were covered by gliotic scar tissue; the nerve fibers were no longer exposed directly to the CSF.

The brains of neonate albino rats were examined with the light and electron microscope following subcutaneous administration of monosodium glutamate (MSG). In addition to lesions in areas known to be vulnerable to glutamate, such as the arcuate nucleus of the hypothalamus, distinct areas of necrotic tissue were detected in the granular portion of the retrosplenial cingulate cortex. The affected cells display the cytological features characteristic of MSG-lesioned brain tissue, including vacuolization of the endoplasmic reticulum and clumping of chromatin. Numerous pyknotic nuclei can be detected as early as 3 h following treatment. The possible causes of the lesion, particularly the role that may be played by astrocytes, are discussed.

Two methods were used to induce a model of experimental hydrocephalus and hydrosyringomyelia in the cat: a) injection of kaolin into the cisterna magna and b) closure of the lateral apertures of the fourth ventricle with cotton swabs. The pathological changes in the brain ventricles and the central canal of the spinal cord were monitored and documented at regular intervals by computed tomography (CT). The CT method is particularly advantageous for studies of this kind because the animals can be examined frequently without risking disturbances in cerebro-spinal fluid dynamics or tissue damage that would result from introduction of contrast media into the ventricular system. Our results and others reported earlier suggest that the dilated central canal acts as a kind of spontaneous CSF deviation route from the ventricles to the subarachnoid space. In spite of the tendency of the animals to recover in a clinical sense, the internal CSF space continued to expand; in cats the disease is progressive, a fact that is readily evident in follow-up CTs. This characteristic indicates that the spontaneous "shunt system" from the fourth ventricle through the dilated central canal to the spinal CSF spaces does not function well enough. Possible explanations for hydrocephalus compensation and the development of hydrosyringomyelia in experimental animals are discussed.