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There is frequently a need for dural grafts to cover defects resulting from retraction, shrinkage, or excision following neurosurgical procedures. Several materials have been evaluated both experimentally and clinically, and then discarded. Collagen, in its various forms, continues to be an area of intense interest. In this study the authors examined the suitability of collagen sponge to effect dural repair. In a 5-year clinical study 102 collagen sponge implants were examined macroscopically and histologically. Graft encapsulation, neomembrane formation, delayed hemorrhage, and foreign body reactions were not found. The porous nature of the collagen sponge encouraged fibroblastic ingrowth and dural repair. Meningocerebral adhesions were present in 11 patients, all of whom had required significant cortical resection or had pia-arachnoid disruption during the initial surgery. Inflammatory cells were seen only in response to infection. Postoperative cerebrospinal fluid leaks developed in only three of 67 patients who underwent an intradural posterior fossa procedure. In a prospective arm of the study involving 459 patients, the wound infection rate using collagen sponge was 6.1%, which compared favorably (p = 0.67) with the 5.7% rate in a similar group of 637 patients in whom collagen sponge had not been used.

Ochratoxins are secondary metabolites of Aspergillus and Penicillium, that are hazardous to health through contamination of dietary foods. Ochratoxin A (OTA) remains the single most potent member of this group of mycotoxins. OTA has a long half-life in humans and is thus easily detected in serum. Dietary intake studies have confirmed link between endemic nephrotoxicity in humans to their daily household intake of OTA. OTA has been reported to contribute to endemic nephrotoxicity and carcinogenicity in humans and animals. OTA produces renal tumours, DNA adducts and chromosomal aberrations in kidneys. OTA may be embryotoxic, teratogenic, and immunotoxic only at doses higher than those causing nephrotoxicity. The incidence of endemic nephrotoxicity has been mostly reported in northeast Europe since the early fifties. Recent studies however have warned that OTA and other toxins, such as aristolochic acid, show very similar renal pathology. There is thus the need for thorough co-occurrence studies on toxin incidence.

Kinins are biologically active peptides that are powerful mediators of cellular inflammation. They mimic the cardinal signs of inflammation by inducing vasodilatation and by increasing vascular permeability and pain. Neutrophils are chemoattracted to sites of inflammation by several stimuli. However, the evidence concerning the chemotactic effect of kinin peptides has been contradictory. We analyzed the chemotactic effect of kinin B(1) receptor agonists on neutrophils isolated from peripheral blood of human healthy subjects. Chemotaxis was performed using the migration under agarose technique. To test the effect of B(1) receptor agonists, each assay was carried out overnight at 37 degrees C in 5% CO(2)-95% air on neutrophils primed with 1 ng/ml interleukin-1beta. Simultaneous experiments were performed using unprimed cells or cells challenged with formyl-Met-Leu-Phe (fMLP). A clear chemotactic activity was observed when primed neutrophils were challenged with Lys-des[Arg(9)]-bradykinin (LDBK) or des[Arg(9)]-bradykinin at 10(-10) M but not when unprimed cells were used. A reduction in the chemotactic response was observed after priming of cells in the presence of 0.5 mM cycloheximide and 10 mug/ml brefeldin A, suggesting that some protein biosynthesis is required. Techniques such as reverse transcriptase-polymerase chain reaction and in situ hybridization confirmed the expression of the B(1) receptor mRNA, and immunocytochemistry and autoradiography demonstrated the expression of the B(1) receptor protein. In contrast to other chemoattractants such as fMLP, cytosolic intracellular calcium did not increase in response to the B(1) receptor agonist LDBK. A generation of kinin B(1) receptor agonists during the early phase of acute inflammation may favor the recruitment of neutrophils to the inflammatory site.

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Colon cancer is the third most common cancer globally. The risk of developing colon cancer is influenced by a number of factors that include age and diet, but is primarily a genetic disease, resulting from oncogene over-expression and tumour suppressor gene inactivation. The induction and progression of the disease is briefly outlined, as are the cellular changes that occur in its progression. While colon cancer is uniformly amenable to surgery if detected at the early stages, advanced carcinomas are usually lethal, with metastases to the liver being the most common cause of death. Oncogenes and genetic mutations that occur in colon cancer are featured. The molecules and signals that act to eradicate or initiate the apoptosis cascade in cancer cells, are elucidated, and these include caspases, Fas, Bax, Bid, APC, antisense hTERT, PUMA, 15-LOX-1, ceramide, butyrate, tributyrin and PPARgamma, whereas the molecules which promote colon cancer cell survival are p53 mutants, Bcl-2, Neu3 and COX-2. Cancer therapies aimed at controlling colon cancer are reviewed briefly.

It was first shown by Ludwig in 1851 that stimulation of the chorda tympani nerve or of the cervical sympathetic chain evoked a secretion of saliva from the submaxillary gland of the cat. Claude Bernard (1858) later showed that, whereas parasympathetic stimulation produced a concomitant vasodilatation, sympathetic stimulation produced vasoconstriction. It was also observed subsequently that a vasodilatation often followed this constriction (Carlson, 1907). Heidenhain (1872) made the interesting observation that although a small dose of atropine completely blocked the secretion produced by stimulation of the chorda tympani nerve, the intense associated vasodilatation was practically unaffected. The latter experiment was performed on dogs but the same phenomenon also occurs in cats (see Burgen & Emmelin, 1961).For many years the view was generally held that there were separate secretory and vasomotor nerve fibres in both the parasympathetic and sympathetic nerves to this gland. The existence of dilator nerve fibres was first challenged by Barcroft and his colleagues (Barcroft & Piper, 1912;Barcroft, 1914) as a consequence of their experiments on the relation between metabolic activity, secretion and blood flow in the submaxillary gland. From these experiments Barcroft (1914) concluded that the vasodilatation which is associated with sympathetic nerve stimulation is entirely secondary to the secretory metabolism. He was somewhat more cautious in dismissing the presence of vasodilator fibres in the chorda tympani nerve, stating: 'It is not impossible that under normal circumstances dilatation may be instituted by dilator fibres and maintained by metabolic products.' Bayliss (1923), who held the view that parasympathetic dilator nerve fibres were responsible for this dilatation, pointed out that although Barcroft's measurements on oxygen consumption and vasodilatation showed that these activities increased at the same time, they