PubMed · 8714369
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1995. Bibliographic update.. https://doi.org/10.1016/0955-2235(95)90002-0
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Renal dysplasia is a clinically important consequence of abnormal nephrogenesis. Various forms are encountered in clinical practice; however, renal dysplasia may represent the final common end point of defects in the normal cascade of fetal kidney development. Typical histopathologic changes characterize renal dysplasia, including architectural distortion, metaplasia, and primitive glomeruli and tubules. Cystic changes are not universal but can be found in most situations. The advent of recent molecular techniques, including gene targeting and positional cloning, has expanded our knowledge of the molecular control of normal mammalian nephrogenesis and with it our understanding of the pathogenesis of renal dysplasia. A defect in the ability of the branching ureteric duct and the undifferentiated metanephric blastema to communicate appears to be the basic underlying principle for the formation of dysplasia. Mutation, defective regulation of transcription, and alteration in spatial or temporal expression of a number of classes of genes, including growth factors, have been implicated in the development of renal dysplasia. Numerous examples, both experimental and in nature, highlight this point.
BACKGROUND: For most solid tumours, surgery remains the most effective primary treatment. Despite apparently curative resection, significant numbers of patients develop secondary disease due to growth of undetected micrometastases. The ability of a tumour to metastasize is related to the degree of angiogenesis it induces. In addition, micrometastases rely on new vessel formation to provide the nutrients necessary for growth. A better understanding of how tumours acquire their blood supply may lead to more effective adjuvant therapies and improve survival following surgery. METHODS: A systematic review of the literature on angiogenesis between 1971 and 1997 was performed using the Medline database to ascertain current thinking on angiogenesis and its relevance in oncological surgery. RESULTS: Angiogenesis is a physiological process subject to autocrine and paracrine regulation which has the potential to become abnormal and play a part in a number of pathological states, including cancer. Increased angiogenic stimuli in the perioperative period, associated with concomitant reduction in tumour-derived antiangiogenic factors following resection of a primary tumour, result in a permissive environment which allows micrometastases to grow. CONCLUSION: Recognition of the role of angiogenesis in metastatic tumour growth represents a significant development in our understanding of tumour biology. The development of antiangiogenic agents offers new promise in the treatment of malignancy. Such agents may prevent or control the development and growth of primary and metastatic tumours.
Regulation of interleukin (IL)-12 production by coexpression of tumor necrosis factor (TNF)-alpha, IL-10, and transforming growth factor (TGF)-beta in human monocytes infected with Mycobacterium tuberculosis H37Ra was analyzed. Also, since IL-12 induces interferon (IFN)-gamma, the effect of IFN-gamma on IL-12 expression was examined. IL-12 mRNA was measured by reverse transcriptase-polymerase chain reaction and IL-12 protein by ELISA. IL-12 p35 mRNA was constitutive and inducible. IL-12 p70 protein paralleled IL-12 p40 protein expression. TNF-alpha protein expression occurred earlier than IL-12 p40 protein but was not required for IL-12 induction. Addition or neutralization of TGF-beta did not significantly alter IL-12 induction. In contrast, recombinant IL-10 reduced IL-12 and neutralization of IL-10 minimally enhanced IL-12. A pronounced increase in IL-12 followed IFN-gamma pretreatment, which selectively up-regulated IL-12 p35 mRNA. Further understanding of operative cytokine networks during M. tuberculosis infection may improve strategies for vaccine development and immunotherapy.